¿Es buena idea recurrir a ChatGPT cuando estamos deprimidos o ansiosos?

Source: The Conversation – (in Spanish) – By Felipe Soto-Pérez, Profesor en Psicopatología y Salud Mental del Departamento de Personalidad, Evaluación y Tratamiento Psicológicos, Universidad de Salamanca

La salud mental es uno de los asuntos que más preocupan hoy en día. Se calcula que cuatro de cada diez personas tendrán un problema de este tipo a lo largo de su vida. De ahí la urgencia de encontrar soluciones validadas por la evidencia científica. Algunas de las soluciones que se barajan tienen que ver con el uso de ChatGPT y otras aplicaciones de inteligencia artificial, propuestas que pueden generar curiosidad pero también dudas y desconfianza.

No es nuevo: el desarrollo tecnológico siempre nos ha hecho sentir algo incómodos. Ya a comienzos del siglo XIX, en un pueblo de Inglaterra llamado Leicestershire, Ned Ludd destruyó algunas máquinas textiles. Entre otras razones, argumentaba que lo hacía porque se oponía a los cambios que traía la nueva maquinaria industrial. A partir de ahí nació el término ludita, que describe a personas que rechazan el desarrollo tecnológico.

En el campo de la salud también han existido “momentos luditas”. Por ejemplo, cuando aparecieron los contestadores automáticos o, más recientemente, cuando se comenzó a utilizar la videollamada para atender pacientes. Incluso los propios profesionales se resistían a las videollamadas hasta que la pandemia de la covid-19 les obligó a utilizarlas. ¡Y menos mal que contamos con esa opción!

¿Cómo utilizan las personas la IA para cuidar su salud mental?

Actualmente, el principal uso que se le da a la lA es con fines de acompañamiento, como un “compañero digital” que nos orienta, escucha nuestros pensamientos y angustias, nos aconseja y al que le contamos secretos. Nos lo pone fácil el hecho de que herramientas como ChatGPT estén disponibles en cualquier momento, parezcan empáticas y, por norma, no critiquen ni respondan negativamente.

Quienes utilizan este tipo de IA no suelen preocuparse por la privacidad o la profundidad emocional, pese a que plantea riesgos por el uso de datos personales y por los sesgos con los que se entrenan las herramientas de IA.

No obstante, debemos admitir también que la IA permite identificar señales de malestar antes de que se agraven. Esto se consigue mediante el análisis de los datos de móviles y weareables que informan de patrones de actividad, pasos, sueño, cantidad de mensajes o veces que se mira el móvil. Este tipo de proceso se llama fenotipado digital y ayuda a anticipar recaídas en depresión o episodios en trastornos graves mediante lo que se llama EMA (Ecological Momentary Assessment o Evaluación Ecológica Momentánea).

También se usan modelos de lenguaje para detectar cambios sutiles en el estado emocional de adolescentes y adultos. Por ejemplo, cuando en los mensajes se detecta un aumento de frases del tipo “estoy mal” o “culpa”, así como en la fluidez verbal o en incoherencias sintácticas. El objetivo es claro: actuar antes de que el problema se convierta en crisis, algo que la atención tradicional no siempre logra.

Asimismo se han publicado estudios iniciales donde chatbots de salud mental se muestran eficaces en reducir síntomas leves de ansiedad y depresión, además de fomentar la reflexión personal y el autocuidado. Su disponibilidad 24/7 los convierte en recursos accesibles y de bajo coste, especialmente útiles en contextos con escasez de servicios profesionales.

La IA se está usando para ampliar terapias como la cognitivo-conductual. Algoritmos inteligentes permiten adaptar ejercicios, monitorizar avances y reforzar aprendizajes. Al mismo tiempo, los modelos de lenguaje abren la puerta a diálogos más naturales y sensibles al contexto. Los resultados de estudios científicos muestran reducciones moderadas en síntomas depresivos, especialmente en jóvenes.

Los terapeutas son más empáticos y flexibles

A pesar de estos avances, los profesionales ofrecen una visión más matizada.Comparaciones entre humanos y chatbots revelan que los terapeutas superan claramente a la IA en dimensiones críticas como la empatía, la flexibilidad y la sintonía emocional. Esto refuerza una idea clave: la IA no sustituirá al profesional, sino que se perfila como una herramienta complementaria.

Por ejemplo, en ansiedad y depresión un bot parece ser efectivo al inicio, pero su efecto desaparece a los tres meses. En paralelo a esta extinción, las personas dejan de utilizarlo, de modo que la adherencia a los apoyos sustentados en IA se ha convertido en uno de los grandes desafíos actuales y futuros a la hora de usarla en salud mental.

Las investigaciones también advierten sobre carencias importantes. Un modelo propone imaginarlo como una pirámide con tres pasos. En la base están la seguridad y la privacidad; después, la fiabilidad y la transparencia; y, solo en la cúspide, la eficacia práctica. Sin embargo, la mayor parte de los estudios se concentran en los niveles superiores y dejan en segundo plano cuestiones básicas como la protección de datos o la gestión del sesgo algorítmico. De hecho, un análisis crítico advierte que la falta de supervisión ética y la escasa formación digital de pacientes y profesionales pueden convertir a estas herramientas más en un riesgo que en un apoyo.

La IA ya está diseñada y avanzando. Los profesionales necesitamos prepararnos para este cambio radical en la forma de abordar los problemas de salud mental.

¿Qué podemos esperar del futuro de la IA en salud mental?

La integración de la inteligencia artificial en nuestra vida cotidiana es ya un hecho. Hace apenas tres años, la mayoría de la gente utilizaba un buscador, mientras que hoy millones de usuarios formulan directamente sus preguntas a un asistente conversacional. La permeabilidad de nuestras actividades diarias a la IA es tan alta que cuesta imaginar un retroceso. Al igual que hace dos décadas los ordenadores ocupaban media mesa y hoy caben en el bolsillo, probablemente en pocos años miraremos atrás y nos parecerá rudimentario haber usado la IA solo a través de texto para hablar de nuestra salud mental.

En este campo, el proceso ya comenzó, pero las perspectivas son claras. Las revisiones recientes señalan que la IA no solo permitirá monitorizar síntomas en tiempo real a través de dispositivos cotidianos, sino que también contribuirá a diagnósticos más precisos y a una atención personalizada. Con sus limitaciones y riesgos, la IA ha llegado para quedarse y desarrollarse.


La versión original de este artículo ha sido publicada en la revista Telos, de Fundación Telefónica.


The Conversation

Felipe Soto-Pérez colabora con Telos, la revista que edita Fundación Telefónica.

Madalin Marian Deliu Dumitru colabora con Telos, la revista que edita Fundación Telefónica.

ref. ¿Es buena idea recurrir a ChatGPT cuando estamos deprimidos o ansiosos? – https://theconversation.com/es-buena-idea-recurrir-a-chatgpt-cuando-estamos-deprimidos-o-ansiosos-267243

Trump is cutting funding to universities with large Hispanic student populations – here’s what to know

Source: The Conversation – USA (2) – By Joseph Morales, University Diversity Officer, Associate Professor of Ethnic Studies, California State University, Chico

A billboard truck criticizing education cuts is parked at Florida International University, an HSI in Miami, in March 2025. John Parra/Getty Images for Students Organizing Now

The Trump administration is trying to eliminate diversity, equity and inclusion programs as part of a broader campaign to end what it calls “wokeness” in American education.

As part of this rollback, the Justice Department announced in July 2025 that it would no longer “defend” the federal definition of Hispanic-Serving Institutions, or HSIs. These are colleges where at least 25% of undergraduates identify as Hispanic or Latino.

This is more than a legal technicality. It reflects the Justice Department’s position that HSI grants violate constitutional protections, putting millions of federal dollars for these schools at risk.

Citing this legal rationale, the Department of Education confirmed in September that it had frozen US$350 million in education grants intended for Minority-Serving Institutions. This includes more than $250 million for HSIs, specifically.

The Education Department argues that these programs amount to racial discrimination because they tie federal grants to students’ racial or ethnic backgrounds.

This echoes the Supreme Court’s decision in 2023, which narrowed how colleges can consider race and ethnicity in admissions.

I serve as the university diversity officer at California State University, Chico, an HSI. I am also an ethnic studies scholar who focuses on equity in higher education.

Advocates for HSIs say ending federal funding would hurt already underfunded colleges, particularly those that serve large numbers of first-generation and low-income students.

A woman with dark hair smiles and stands in front of a whiteboard that says in marker, 'HSI week, Sept 9-15'
Elisa Castillo is the assistant vice president for Hispanic Serving Institution and Minority Serving Institution initiatives at Salem State University, a newly designated HSI in Salem, Mass.
Pat Greenhouse/The Boston Globe via Getty Images

What are Hispanic-Serving Institutions?

Congress created the HSI designation in 1992, through an amendment to the 1965 Higher Education Act. This amendment authorizes federal grants to help strengthen colleges that enroll large numbers of Hispanic and low-income students, providing more opportunity for those students to succeed and graduate.

There are more than 600 federally designated HSIs across the U.S. and Puerto Rico. California is home to the most HSIs, with 167, followed by Texas, Puerto Rico, New York and Illinois.

In addition to showing that at least 25% of its student population is Hispanic or Latino, any college or university that wants to qualify as an HSI must also show that at least half of its students come from low-income backgrounds.

Becoming an HSI allows colleges and universities to apply for federal funding intended to support underrepresented and low-income students.

HSIs vary in size and mission

HSIs enroll over 1.5 million Hispanic students, which amounts to over 60% of all Hispanic undergraduates in the U.S.

This marks a big increase from the 340,000 Hispanic undergraduates who attended an HSI in 1995.

Some of these schools are large public research universities, such as University of California, Riverside; University of California, Santa Barbara; and University of California, Santa Cruz. Others are regional institutions, private colleges and local community colleges.

Over the past decade, another kind of Hispanic-Serving Institution has emerged – research-intensive HSIs. These are colleges and universities where at least 25% of the student body is Hispanic and where there is significant research funding and a range of doctoral programs offered. These schools include University of California, Irvine; Florida International University; and the University of Texas at El Paso, among others.

Some researchers have debated whether the HSI category has become too broad, grouping schools with vastly different resources, missions and student populations.

Despite their differences, many HSIs enroll large numbers of first-generation, low-income and working students, as well as immigrants and transfer students.

HSIs also generally operate with fewer financial and academic resources than comparable non-HSI institutions.

How HSI funding works

Title V grants from the Department of Education are one clear way that HSIs can receive federal funding .

These competitive grants are intended to help HSIs expand educational opportunities and institutional capacity to support Hispanic and low-income students.

Rather than providing aid directly to students, Title V grants are used to offer faculty training, update classrooms and laboratories, create new degree programs and develop mentorship opportunities for first-generation students.

At campuses such as California State University, Chico and University of California, Irvine, Title V grants have given schools the money to create bilingual advising services and maintain data systems.

Title V grants form only one part of the broader funding picture for HSIs. Like many colleges, HSIs rely on state funding and tuition revenue. They also compete for other federal grants, including those from the National Science Foundation and the Department of Agriculture.

How HSIs help Hispanic students

A growing body of research shows that HSIs are crucial in helping more Hispanic and first-generation students attend and graduate college.

Some HSIs have received national recognition for using evidence-based practices to help Hispanic students perform better in the classroom. Hispanic students at these schools, which include Arizona State University and California State University, Fullerton, graduate at rates roughly 8 percentage points higher than Hispanic students nationally.

Hispanic students at HSIs graduate at rates more than 5 percentage points higher than those at comparable non-HSI colleges, according to similar 2017 findings from the nonprofit Education Trust.

There are a few reasons why there is a relatively high graduation rate for Hispanic students at HSIs.

Students at HSIs often report feeling a strong sense of belonging and see their own cultures reflected in the curriculum. Many HSI campuses also offer dedicated programs for first-generation students and train faculty to teach and advise with equity and inclusion in mind.

At University of California, Irvine, where I helped lead HSI initiatives, Hispanic undergraduate enrollment grew by nearly 150% between 2009 and 2019, from 3,000 students to more than 7,500.

During that time, more than 350 faculty and staff completed equity-focused training to strengthen advising and teaching practices that support Hispanic and other underrepresented students.

People hold umbrellas and walk together in the rain near palm trees, in front of a large sign that days Fullerton
Visitors to California State University, Fullerton take a guided campus tour.
Jeff Gritchen/MediaNews Group/Orange County Register via Getty Images

What’s at stake for HSIs

Hispanic Americans now make up nearly 20% of the U.S. population, and their college enrollment numbers are projected to grow from about 3.7 million in 2020 to 4.5 million by 2030, as overall college enrollment numbers are projected to decline during this time.

A national evaluation of Title V projects found that most colleges and universities used these grants to improve student services, develop new academic programs and build community partnerships that help first-generation and low-income students stay enrolled and complete their degrees.

As HSI researchers note, graduation rates tell only part of the story. True student success at HSIs depends not just on graduation numbers, but on culturally responsive teaching, inclusive campus climates and equity-minded institutional practices.

How policymakers define and fund HSIs will shape not only the future of these institutions but also whether this growing generation of Hispanic students can access, afford and complete college in the years ahead.

The Conversation

Joseph Morales, Ph.D., works at California State University, Chico, a federally designated Hispanic-Serving Institution (HSI). While not a principal investigator on any federal HSI grants, he has participated in professional development programs and national conferences hosted by organizations mentioned in the article, including the Hispanic Association of Colleges and Universities (HACU). These experiences inform his understanding of the field but did not influence the content of this piece. The views expressed are those of the author and do not necessarily reflect the views of California State University, Chico.

ref. Trump is cutting funding to universities with large Hispanic student populations – here’s what to know – https://theconversation.com/trump-is-cutting-funding-to-universities-with-large-hispanic-student-populations-heres-what-to-know-251202

Can you really be addicted to food? Researchers are uncovering convincing similarities to drug addiction

Source: The Conversation – USA (3) – By Claire Wilcox, Adjunct Faculty in Psychiatry, University of New Mexico

Research has found that high-sugar, ultraprocessed foods can be addictive for some people. Doucefleur/iStock via Getty Images Plus

People often joke that their favorite snack is “like crack” or call themselves “chocoholics” in jest.

But can someone really be addicted to food in the same way they could be hooked on substances such as alcohol or nicotine?

As an addiction psychiatrist and researcher with experience in treating eating disorders and obesity, I have been following the research in this field for the past few decades. I have written a textbook on food addiction, obesity and overeating disorders, and, more recently, a self-help book for people who have intense cravings and obsessions for some foods.

While there is still some debate among psychologists and scientists, a consensus is emerging that food addiction is a real phenomenon. Hundreds of studies have confirmed that certain foods – often those that are high in sugar and ultraprocessedaffect the brains and behavior of certain people similarly to other addictive substances such as nicotine.

Still, many questions remain about which foods are addictive, which people are most susceptible to this addiction and why. There are also questions as to how this condition compares to other substance addictions and whether the same treatments could work for patients struggling with any kind of addiction.

How does addiction work?

The neurobiological mechanisms of addiction have been mapped out through decades of laboratory-based research using neuroimaging and cognitive neuroscience approaches.

Studies show that preexisting genetic and environmental factors set the stage for developing an addiction. Regularly consuming an addictive substance then causes a rewiring of several important brain systems, leading the person to crave more and more of it.

This rewiring takes place in three key brain networks that correspond to key functional domains, often referred to as the reward system, the stress response system and the system in charge of executive control.

First, using an addictive substance causes the release of a chemical messenger called dopamine in the reward network, which makes the user feel good. Dopamine release also facilitates a neurobiological process called conditioning, which is basically a neural learning process that gives rise to habit formation.

As a result of the conditioning process, sensory cues associated with the substance start to have increasing influence over decision-making and behavior, often leading to a craving. For instance, because of conditioning, the sight of a needle can drive a person to set aside their commitment to quit using an injectable drug and return to it.

Second, continued use of an addictive substance over time affects the brain’s emotional or stress response network. The user’s body and mind build up a tolerance, meaning they need increasing amounts of the substance to feel its effect. The neurochemicals involved in this process are different than those mediating habit formation and include a chemical messenger called noradrenaline and internally produced opioids such as endorphins. If they quit using the substance, they experience symptoms of withdrawal, which can range from irritability and nausea to paranoia and seizures.

At that point, negative reinforcement kicks in. This is the process by which a person keeps going back to a substance because they’ve learned that using the substance doesn’t just feel good, but it also relieves negative emotions. During withdrawal from a substance, people feel profound emotional discomfort, including sadness and irritability. Negative reinforcement is why someone who is trying to quit smoking, for instance, will be at highest risk of relapse in the week just after stopping and during times of stress, because in the past they’d normally turn to cigarettes for relief.

Third, overuse of most addictive substances progressively damages the brain’s executive control network, the prefrontal cortex, and other key parts of the brain involved in impulse control and self-regulation. Over time, the damage to these areas makes it more and more difficult for the user to control their behavior around these substances. This is why it is so hard for long-term users of many addictive substances to quit.

Scientists have learned more about what’s happening in a person’s brain when they become addicted to a substance.

What evidence is there that food is addictive?

Many studies over the past 25 years have shown that high-sugar and other highly pleasurable foods – often foods that are ultraprocessed – act on these brain networks in ways that are similar to other addictive substances. The resulting changes in the brain fuel further craving for and overuse of the substance – in this case, highly rewarding food.

Clinical studies have demonstrated that people with an addictive relationship to food demonstrate the hallmark signs of a substance use disorder.

Studies also indicate that for some people, cravings for highly palatable foods go well beyond just a normal hankering for a snack and are, in fact, signs of addictive behavior. One study found that cues associated with highly pleasurable foods activate the reward centers in the brain, and the degree of activation predicts weight gain. In other words, the more power the food cue has to capture a person’s attention, the more likely they are to succumb to cravings for it.

Multiple studies have also found that suddenly ending a diet that’s high in sugar can cause withdrawal, similar to when people quit opioids or nicotine.

Excessive exposure to high-sugar foods has also been found to reduce cognitive function and cause damage to the prefrontal cortex and hippocampus, the parts of the brain that mediate executive control and memory.

In another study, when obese people were exposed to food and told to resist their craving for it by ignoring it or thinking about something else, their prefrontal cortexes were more active compared with nonobese individuals. This indicates that it was more difficult for the obese group to fight their cravings.

drawing of a woman in a spiral surrounded by processed foods
Researchers are still working out the best methods to help patients with food addictions develop a healthy relationship with food.
Viktar Sarkisian/iStock via Getty Images Plus

Finding safe treatments for patients struggling with food

Addiction recovery is often centered on the idea that the fastest way to get well is to abstain from the problem substance. But unlike nicotine or narcotics, food is something that all people need to survive, so quitting cold turkey isn’t an option.

In addition, eating disorders such as bulimia nervosa and binge-eating disorder often occur alongside addictive eating. Most psychologists and psychiatrists believe these illnesses have their root cause in excessive dietary restriction.

For this reason, many eating disorder treatment professionals balk at the idea of labeling some foods as addictive. They are concerned that encouraging abstinence from particular foods could trigger binge eating and extreme dieting to compensate.

A way forward

But others argue that, with care, integrating food addiction approaches into eating disorders treatment is feasible and could be lifesaving for some.

The emerging consensus around this link is moving researchers and those who treat eating disorders to consider food addiction in their treatment models.

One such approach might look like the one described to me by addiction psychiatrist and eating disorders specialist Dr. Kim Dennis. In line with traditional eating disorder treatment, nutritionists at her residential clinic strongly discourage their patients from restricting calories. At the same time, in line with traditional addiction treatment, they help their patients to consider significantly reducing or completely abstaining from particular foods to which they have developed an addictive relationship.

Additional clinical studies are already being carried out. But going forward, more studies are needed to help clinicians find the most effective treatments for people with an addictive relationship with food.

Efforts are underway by groups of psychologists, psychiatrists, neuroscientists and mental health providers to get “ultraprocessed food use disorder,” also known as food addiction, into future editions of diagnostic manuals such as the Diagnostic and Statistical Manual of Mental Disorders and the World Health Organization’s International Classification of Diseases.

Beyond acknowledging what those treating food addiction are already seeing in the field, this would help researchers get funding for additional studies of treating food addiction. With more information about what treatments will work best for whom, those who have these problems will no longer have to suffer in silence, and providers will be better equipped to help them.

The Conversation

I have two books for sale which address food addiction, and I could benefit financially from increased interest in the food addiction topic:

Wilcox C.E. Food Addiction Obesity and Disorders of Overeating: An Evidenced Based Assessment and Clinical Guide. (2021) Springer

Wilcox C. Rewire Your Food-Addicted Brain: Fight Cravings and Break Free from a High-Sugar Ultra-Processed Diet. (2025) New Harbinger Publications

ref. Can you really be addicted to food? Researchers are uncovering convincing similarities to drug addiction – https://theconversation.com/can-you-really-be-addicted-to-food-researchers-are-uncovering-convincing-similarities-to-drug-addiction-261727

Flu season has arrived – and so have updated flu vaccines

Source: The Conversation – USA (3) – By Libby Richards, Professor of Nursing, Purdue University

The flu vaccine is updated every year to include the strains known to be circulating. Cecilie_Arcurs/E+ via Getty Images

As the autumn’s cool weather settles in, so does flu season – bringing with it the familiar experiences of sniffles, fever and cough.

Every year, influenza – the flu – affects millions of people. Most will experience the infection as a mild to moderate illness – but for some, it can be severe, potentially resulting in hospitalization and even death.

While the start of flu season may feel routine, it’s important to remember that the virus changes every year, making annual vaccination an important part of staying healthy.

What to expect this flu season

Public health experts are closely watching how this year’s flu season unfolds. Early reports suggest that the U.S. may see a moderate level of flu cases, partly because last year’s flu activity was high and it’s uncommon to have two severe flu seasons in a row.

However, the U.S. also uses data from the Southern Hemisphere’s earlier flu season, which lasts from April to October, to help predict what the season might look like. There, the flu season has been more severe than in years past.

Taken together, that means there could be a significant number of flu cases in the U.S., particularly among children, older adults and those with chronic health conditions.

Each year, the flu vaccine is updated to best match the strains of influenza expected to circulate. Because flu viruses mutate frequently, the effectiveness of the flu vaccine can vary each year. However, even when the match between the seasonal flu and the vaccine that is designed around it isn’t perfect, vaccination remains the best protection against severe illness.

In the U.S., all flu vaccines for the 2025-2026 season will be trivalent – which means they are formulated to protect against the three main groups of influenza virus strains. These are an A (H1N1) virus, an A (H3N2) virus and a B/Victoria virus.

A family, mom, dad and two young children all sit in bed together blowing their noses.
The flu vaccine protects against severe illness from an influenza infection.
Jacob Wackerhausen/iStock via Getty Images Plus

Vaccine availability

Recent vaccine policy changes have created some confusion, particularly around COVID-19 vaccines. Many people are wondering if getting the flu vaccine has become more complicated. The good news is that flu vaccines remain widely available and accessible. Pharmacies, doctors’ offices, public health clinics and many workplaces are offering the seasonal shot, often at little or no cost.

The 2025-2026 flu vaccine is available now. Manufacturers start shipping vaccines doses in July and August to ensure access by September. While public health experts won’t know the exact effectiveness of the flu vaccine until flu season is over, the flu shot usually cuts your chances of needing to see a doctor for the flu by about half.

Vaccination helps reduce the severity of illness, the likelihood of hospitalization and the spread of infection within our communities.

It’s important to note that you can get the flu shot at the same time as other vaccines, such as the COVID-19 vaccine or the RSV and pneumonia vaccines for older adults, without compromising effectiveness. If you’re unsure which vaccines are right for you, your health care provider or pharmacist can help you decide based on your age and health status.

Who should get the flu shot

The Centers for Disease Control and Prevention recommends that everyone 6 months and older receive the flu vaccine each year, with rare exceptions. That aligns with guidelines from other organizations, such as the American Association of Pediatrics.

The flu vaccine is especially important for:

• Adults 65 and older

• Children under 5 – and particularly those under 2

• Pregnant people

• People with chronic conditions such as asthma, diabetes or heart disease

• Health care workers and caregivers

Even if you’re healthy and rarely get sick, getting vaccinated protects not only you but also those around you who may be more vulnerable.

Practical prevention tips

In addition to vaccination, everyday actions help reduce the spread of flu and other respiratory viruses:

Wash your hands frequently with soap and water.

• Cover your coughs and sneezes.

• Stay home if you’re feeling unwell.

• Consider wearing a mask in crowded indoor spaces during peak flu activity, particularly if you have a cough.

Even though flu season is part of life, serious illness doesn’t have to be. By staying informed, getting vaccinated and practicing healthy habits, everyone can play a role in keeping their communities safe and healthy.

If you haven’t gotten your flu shot yet, now’s the time to protect yourself, and those you care for, this flu season.

The Conversation

Libby Richards has received funding from the American Nurses Foundation, National Institutes of Health, and the Indiana Clinical and Translational Sciences Institute .

ref. Flu season has arrived – and so have updated flu vaccines – https://theconversation.com/flu-season-has-arrived-and-so-have-updated-flu-vaccines-267058

How pollution and the microbiome interact with Tregs, the immune system regulators whose discovery was honored with the Nobel Prize

Source: The Conversation – USA (3) – By Prakash Nagarkatti, Professor of Pathology, Microbiology and Immunology, University of South Carolina

Treg cells have been thrust into the limelight thanks to the Nobel Prize-winning work of a team of researchers from the U.S. and Japan. jarun011/iStock via Getty Images Plus

A special group of immune cells known as regulatory T cells, or Tregs for short, became an overnight sensation when a trio of U.S. and Japanese scientists won the Nobel Prize in physiology or medicine on Oct. 6, 2025, for their discovery and elucidation of these cells.

Treg cells act as the “master regulators” of the immune system – much like conductors leading an orchestra – ensuring that all other immune cells work in harmony. People with too few or defective Treg cells often develop autoimmune diseases, where unchecked immune cells mistakenly attack the body’s own tissues or organs. Yet when Treg cells become too numerous, people can become more susceptible to cancer and infections.

For this reason, Treg cells are often described as a double-edged sword. Treg cells also control internal revolt in the form of an overactive immune response by other immune cells that can trigger allergies and autoimmune diseases such as arthritis, lupus and multiple sclerosis – diseases that develop when Treg cells are defective in either number, function or both.

The well-established functions of Treg cells in autoimmune diseases, cancer and infections have recently been complemented by research unraveling how environmental factors influence these cells and modulate the immune response.

We are a husband-wife team of immunologists who study how environmental factors such as chemicals, diet and gut bacteria affect Treg cells and the overall functioning of the immune system.

While our study dating back to 1984 found that certain environmental contaminants induce T cells that suppress the immune system, further study on such cells was hampered by an inability in the field at large to isolate and characterize these cells. The discoveries honored by this year’s Nobel Prize transformed how researchers understand the immune system.

Nobel-Prizing winning scientist showing extreme emotion.
One of the three Nobel Prize-winning researchers, Mary E. Brunkow, responds emotionally as she receives the news of the prize.
AP Photo/Lindsey Wasson

The interplay of environmental factors

The environment plays a profound role in regulating the development, maintenance and functions of Treg cells. Some examples of environmental factors include chemical pollutants found in the air and water, microbes, sunlight, diet and medications.

Rather than being a single, static population, Treg cells are highly adaptable. They integrate a variety of environmental cues to either suppress or manage immune responses. They accomplish this by producing key molecules such as FoxP3 that send a signal to other immune cells to stop mounting an aggressive immune response.

Certain toxic chemicals can increase the number or activity of Treg cells. One of the best-known examples is a group of long-lasting pollutants called dioxins that accumulate in fatty tissues through consumption of contaminated meat, dairy and fish. They are produced from burning waste as well as chemical manufacturing and forest fires.

The most toxic dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin, or TCDD, is a known human carcinogen. Researchers have linked exposure to this chemical to various health problems, including cancer and reproductive and developmental issues. Research shows that dioxins activate Treg cells through a sensor known as the aryl hydrocarbon receptor. This constitutes one of the mechanisms through which certain environmental chemicals promote cancer by enhancing Treg activity and suppressing the anti-cancer immune response.

Air pollution, such as diesel exhaust, can have the opposite effect, impairing Treg cell function and contributing to inflammatory diseases such as asthma. This may occur through damage to the FoxP3 gene.

Colorful illustration of five types of T cells against a white background.
Regulatory T cells, or Treg cells, are one of at least five major types of T cells.
ttsz/iStock via Getty Images Plus

How diet interacts with Treg cells

Diet also plays a powerful role in regulating Treg cells. Compounds known as indoles, found in vegetables from the cabbage family such as broccoli, cabbage and cauliflower, can activate Treg cells and help prevent gut inflammation. These compounds also work by stimulating the aryl hydrocarbon receptor, which boosts Treg numbers and activity.

Another way diet can influence Treg cells is through the regulation of the microbes that live in the gut.

The gut has trillions of microbial residents, both benefical and harmful. Previous research found that Treg cells in the gut play a crucial role in maintaining gut homeostasis – the dynamic balance between microbiota and immune cells found in the gut. Any disturbance leading to loss of Treg cell function can lead to hyperactivation of other immune cells in the gut. This can trigger inflammation in which the immune cells destroy the lining of the intestine, leading to conditions such as inflammatory bowel disease.

Other naturally occurring substances – such as naringenin, a chemical abundant in citrus fruits, and epigallocatechin-3-gallate, a compound found in green tea – also activate the aryl hydrocarbon receptor and promote Treg development.

A fiber-rich diet supports the growth of beneficial gut bacteria. This bacteria ferments fiber into short-chain fatty acids that enhance Treg cell function and help maintain gut health. Probiotic bacteria also increases Treg cell populations, thereby reducing inflammation.

In addition, dietary tryptophan – an amino acid found in foods such as poultry, eggs, tofu and seeds – is metabolized into compounds that activate the aryl hydrocarbon receptor, further boosting Treg cell activity and protecting against gut inflammation.

By contrast, a Western diet high in fat, sugar and processed foods disrupts the balance of gut bacteria. This, in turn, reduces the population of microbes that support Treg cells and promotes a more inflammatory environment in the gut.

Keeping Treg cells in harmony

Scientists like us and many others are working to understand the processes involved in maintaining the delicate balance of Treg cells that are influenced by all of these outside factors. The goal is to learn how Treg cells and other immune cells can be kept in equilibrium – strong enough to defend against infections and cancer yet restrained enough to prevent autoimmune and inflammatory diseases.

The profound environmental influence on Treg cell development and function makes understanding these interactions crucial for defining the fine line between health and disease.

The Conversation

Prakash Nagarkatti receives funding from the National Institutes of Health.

Mitzi Nagarkatti receives funding from the National Institutes of Health.

ref. How pollution and the microbiome interact with Tregs, the immune system regulators whose discovery was honored with the Nobel Prize – https://theconversation.com/how-pollution-and-the-microbiome-interact-with-tregs-the-immune-system-regulators-whose-discovery-was-honored-with-the-nobel-prize-266865

The new president of The Church of Jesus Christ of Latter-day Saints will inherit a global faith far more diverse than many realize

Source: The Conversation – USA (3) – By Brittany Romanello, Assistant Professor of Sociology, University of Arkansas

Missionary Sayon Ang holds up a sign signifying she speaks Cambodian during the twice-annual conference of The Church of Jesus Christ of Latter-day Saints on Oct. 4, 2014, in Salt Lake City. AP Photo/Kim Raff

The Church of Jesus Christ of Latter-day Saints has spent the past few weeks in a moment of both mourning and transition. On Sept. 28, 2025, a shooting and arson at a Latter-day Saints meetinghouse in Michigan killed four people and wounded eight more. What’s more, Russell M. Nelson, president of the church, died the day before at age 101. Based on protocol, his role will most likely be filled by Dallin H. Oaks, the longest-serving of the church’s top leaders.

The next president will inherit leadership of a religious institution that is both deeply American and increasingly global – diversity at odds with the way it’s typically represented in mainstream media, from “The Secret Life of Mormon Wives” to “The Book of Mormon” Broadway musical.

As a cultural anthropologist and ethnographer, I research Latter-day Saints communities across the United States, particularly Latina immigrants and young adults. When presenting my research, I’ve noticed that many people still closely associate the church with Utah, where its headquarters are located.

An ornate white building with a tall spire, and green mountains in the background.
The Latter-day Saints temple in Cochabamba, Bolivia, was dedicated in 2000.
Parallelepiped09/Wikimedia Commons, CC BY-SA

The church has played a pivotal role in Utah’s history and culture. Today, though, only 42% of its residents are members. The stereotype of Latter-day Saints as mostly white, conservative Americans is just one of many long-standing misconceptions about LDS communities and beliefs.

Many people are surprised to learn there are vibrant congregations far from the American West’s “Mormon Corridor.” There are devout Latter-day Saints everywhere from Ghana and the United Arab Emirates to Russia and mainland China.

Global growth

Joseph Smith founded The Church of Jesus Christ of Latter-day Saints in upstate New York in 1830 and immediately sent missionaries to preach along the frontier. The first overseas missionaries traveled to England in 1837.

Shortly after World War II, church leaders overhauled their missionary approach to increase the number of international missions. This strategy led to growth across the globe, especially in Central America, South America and the Pacific Islands.

Today, the church has over 17.5 million members, according to church records. A majority live outside the U.S., spread across more than 160 countries.

One way the church and researchers track this global growth is by construction of new temples.These buildings, used not for weekly worship but special ceremonies like weddings, were once almost exclusively located in the United States. Today, they exist in dozens of countries, from Argentina to Tonga.

During Nelson’s presidency, which began in 2018, he announced 200 new temples, more than any of his predecessors. Temples are a physical and symbolic representation of the church’s commitment to being a global religion, although cultural tensions remain.

Two men in suits walk by a large map of the world framed on the wall of a hallway.
Two missionaries for The Church of Jesus Christ of Latter-day Saints walk through the Missionary Training Center in Provo, Utah, in 2008.
AP Photo/George Frey

Among U.S. members, demographics are also shifting. Seventy-two percent of American members are white, down from 85% in 2007, according to the Pew Research Center. Growing numbers of Latinos – 12% of U.S. members – have played a significant role sustaining congregations across the country.

There are congregations in every U.S. state, including the small community of Grand Blanc, Michigan, site of the tragic shooting. Suspect Thomas Jacob Sanford, who was fatally shot by police, had gone on a recent tirade against Latter-day Saints during a conversation with a local political candidate.

In the following days, an American member of the church raised hundreds of thousands of dollars for Sanford’s family.

Growing pains

Despite the church’s diversity, its institutional foundations remain firmly rooted in the United States. The top leadership bodies are still composed almost entirely of white men, and most are American-born.

As the church continues to grow, questions arise about how well the norms of a Utah-based church fit the realities of members in Manila or Mexico City, Bangalore or Berlin. How much room is there, even in U.S. congregations, for local cultural expressions of faith?

Latino Latter-day Saints and members in Latin America, for example, have faced pushback against cultural traditions that were seen as distinctly “not LDS,” such as making altars and giving offerings during Dia de los Muertos. In 2021, the church launched a Spanish-language campaign using Day of the Dead imagery to increase interest among Latinos. Many members were happy to see this representation. Still, some women I spoke with said that an emphasis on whiteness and American nationalism, as well as anti-immigrant rhetoric they’d heard from other members, deterred them from fully celebrating their cultures.

A couple dressed nicely and holding hands walks by a large portrait of Jesus, portrayed as a bearded white man, inside a large hallway.
People attend the twice-annual conference of The Church of Jesus Christ of Latter-day Saints on April 6, 2024, in Salt Lake City.
AP Photo/Rick Bowmer

Even aesthetic details, like musical styles, often reflect a distinctly American model. The standardized hymnal, for example, contains patriotic songs like “America the Beautiful.” This emphasis on American culture can feel especially out of sync in places in countries with high membership rates that have histories of U.S. military or political interventions.

Expectations about clothing and physical appearance, too, have prompted questions about representation, belonging and authority. It was only in 2024, for instance, that the church offered members in humid areas sleeveless versions of the sacred garments Latter-day Saints wear under clothing as a reminder of their faith.

Historically, the church viewed tattoos as taboo – a violation of the sanctity of the body. Many parts of the world have thousands of years of sacred tattooing traditions – including Oceania, which has high rates of church membership.

Change ahead?

Among many challenges, the next president of the church will navigate how to lead a global church from its American headquarters – a church that continues to be misunderstood and stereotyped, sometimes to the point of violence.

A white building in the distance, with palm trees and a clear reflecting pool in the foreground.
The temple in Laie, Hawaii, opened in the early 1900s, making it one of the church’s oldest.
Kaveh/Wikimedia Commons, CC BY-SA

The number of Latter-day Saints continues to grow in many parts of the world, but this growth brings a greater need for cultural sensitivity. The church, historically very uniform in its efforts to standardize Latter-day Saints history, art and teachings, is finding that harder to maintain when congregations span dozens of countries, languages, customs and histories.

Organizing the church like a corporation, with a top-down decision-making process, can also make it difficult to address painful racial histories and the needs of marginalized groups, like LGBTQ+ members.

The transition in leadership offers an opportunity not only for the church but for the broader public to better understand the multifaceted, global nature of Latter-day Saints’ lives today.

The Conversation

Brittany Romanello does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

ref. The new president of The Church of Jesus Christ of Latter-day Saints will inherit a global faith far more diverse than many realize – https://theconversation.com/the-new-president-of-the-church-of-jesus-christ-of-latter-day-saints-will-inherit-a-global-faith-far-more-diverse-than-many-realize-266337

Entretien avec Simon Sakaguchi, prix Nobel de médecine

Source: The Conversation – France in French (3) – By Gemma Ware, Host, The Conversation Weekly Podcast, The Conversation

Dans les années 1980, Shimon Sakaguchi, alors jeune chercheur en immunologie, peinait à obtenir des financements pour ses recherches. Aujourd’hui, ses travaux pionniers, qui ont permis de lever le voile sur la façon dont notre système immunitaire détermine à quoi s’attaquer (et à quel moment), viennent d’être récompensés par le prix Nobel de physiologie ou médecine. Dans cet entretien, il revient sur cette découverte majeure et ses implications médicales.


Le 6 octobre 2025, le Japonais Shimon Sakaguchi et les Américains Mary Brunkow et Fred Ramsdell se sont vus décerner le prix Nobel de physiologie ou médecine pour leurs travaux sur les lymphocytes T régulateurs (aussi appelés lymphocytes Treg), une classe particulière de cellules immunitaires qui empêchent notre système immunitaire de s’en prendre à notre propre corps.

Dans cet épisode du podcast The Conversation Weekly, Shimon Sakaguchi nous raconte comment il est parvenu à cette découverte, ainsi que son intérêt médical.

La transcription en francais de ce podcast est disponible en bas de cette page.


L’histoire commence par une intuition, née à la suite d’expérimentations réalisées par des collègues de Shimon Sakaguchi, au sein de l’Institut de recherche sur le cancer d’Aichi, à Nagoya. Ces derniers avaient procédé à l’ablation du thymus des souris nouvellement nées, trois jours après leur naissance. On savait déjà à cette époque que ce petit organe, situé derrière le haut du sternum chez l’être humain, jouait un rôle important dans le développement de l’autotolérance immunitaire. C’est en effet dans le thymus que les lymphocytes T qui risqueraient de s’attaquer à l’organisme sont isolés et détruits.

Si l’on retire le thymus d’une souris normale pendant la période néonatale, il semblait logique de s’attendre à ce qu’elle présente une déficience immunitaire, car ses lymphocytes auraient dû avoir disparu. Mais c’est exactement le contraire qui s’est produit chez les souris dont on avait ôté le thymus : elles ont développé des maladies auto-immunes, autrement dit des maladies au cours desquelles le système immunitaire s’en prend au corps qu’il est censé protéger. Ces maladies se sont avérées très similaires à celles observées chez l’être humain.

Ce résultat a intrigué Shimon Sakaguchi. En effet, contrairement aux souris opérées par ses collègues, les patients victimes de maladies auto-immunes possèdent toujours leur thymus. Le chercheur a alors émis l’hypothèse de l’existence d’un mécanisme commun entre les deux situations, qui expliquerait à la fois la survenue de maladies auto-immunes spontanées chez l’être humain, et le fait que des souris auxquelles on a enlevé le thymus développent néanmoins des maladies auto-immunes.

Via une nouvelle expérience, Shimon Sakaguchi a tenté d’empêcher l’emballement du système immunitaire de souris dépourvues de thymus. Pour cela, il a prélevé des lymphocytes T sur des souris génétiquement identiques aux souris opérées, et les a réinjectées à ces dernières. Ainsi traitées, les souris sans thymus ne développaient plus de maladie auto-immune. Conclusion du chercheur : « Cela suggérait qu’il devait exister une population de lymphocytes T capable d’empêcher le développement de ces maladies ».

Mais dans les années 1980, obtenir des fonds pour mener de telles recherches n’était pas chose aisée, car « la communauté des spécialistes en immunologie était très sceptique quant à l’existence de telles cellules », explique Shimon Sakaguchi. Parti pour plusieurs années aux États-Unis, le chercheur reconnaît avoir eu « beaucoup de chance » lorsqu’une fondation privée a accepté de soutenir ses travaux.

Dix ans de recherche supplémentaires ont été nécessaires avant qu’il puisse publier, en 1995, un article scientifique relatant sa découverte des lymphocytes T régulateurs. On sait aujourd’hui que ceux-ci sont en quelque sorte les agents de sécurité de l’organisme. Ils contrôlent les réactions indésirables et maintiennent l’équilibre du système immunitaire via un processus appelé tolérance périphérique. Leur dysfonctionnement peut être à l’origine de maladies auto-immunes. Les travaux ultérieurs de Shimon Sakaguchi et de ses co-récipiendaires du prix Nobel, Mary Brankow et Fred Ramsdell, ont permis de découvrir le gène Foxp3, qui contrôle spécifiquement les lymphocytes Treg.

Des maladies auto-immunes aux cancers, un fort potentiel

Au début de sa carrière,Shimon Sakaguchi s’intéressait aux maladies auto-immunes et à leurs origines. « Mais au fil de mes recherches, nous avons progressivement compris que les lymphocytes Treg constituaient un sujet plus important », souligne-t-il. On sait désormais que ces cellules sont impliquées dans la manière dont se développent les cancers, ainsi que dans la tolérance du greffon, en cas de transplantation d’organe.

Shimon Sakaguchi et ses collaborateurs travaillent également sur de nouvelles façons d’exploiter les lymphocytes Treg à des fins thérapeutiques, ainsi que sur la mise au point de protocoles permettant de convertir les lymphocytes T « auto-agressifs » en lymphocytes Treg, ce qui permettait espèrent de cibler spécifiquement les maladies auto-immunes dont ils sont responsables.

Son espoir est que, parmi les nombreux essais cliniques actuellement en cours dans le domaine de l’immunothérapie anticancéreuse en lien avec ces travaux, certains aboutissent à des solutions concrètes pour améliorer la prise en charge des patients. Il est également fasciné par de récents résultats de recherche qui suggèrent que les lymphocytes Treg seraient aussi impliqués dans les maladies liées à l’inflammation. Pour influer sur le potentiel de réparation des tissus endommagés, il pourrait être intéressant d’agir sur eux : « Les maladies neurodégénératives telles que la maladie d’Alzheimer ou la maladie de Parkinson sont associées à une inflammation. En ciblant uniquement ce type d’inflammation, nous pourrions peut-être [parvenir à] arrêter la progression de la maladie ou la retarder. Nous espérons que cette piste s’avérera réelle », conclut-il.


Cet épisode de The Conversation Weekly a été produit par Mend Mariwany et Katie Flood et est animé par Gemma Ware. Le mixage et la conception sonore ont été réalisés par Michelle Macklem et la musique du générique par Neeta Sarl.


Traduction française :


TC : Notre système immunitaire est une merveilleuse mécanique. Il est composé de nombreuses composantes qui interagissent, en particulier les anticorps et les lymphocytes T (des cellules immunitaires de type « globules blancs » qui interviennent à la fois dans la destruction des cellules infectées, la coordination de la réponse immunitaire et la mémorisation des infections). Ils nous protègent lorsque nous contractons une infection virale comme le Covid-19 ou la grippe, ou lorsque la consommation d’un curry douteux déclenche une intoxication alimentaire.

Mais chez certaines personnes, le système immunitaire dysfonctionne et s’emballe. Au lieu de cibler les bactéries ou les virus qui les menacent, il s’attaque à leur organisme, s’en prenant à leurs propres cellules. Quand cela arrive, des maladies auto-immunes peuvent se développer, telles que la polyarthrite rhumatoïde ou le diabète de type 1.

Comment notre système immunitaire sait-il contre quoi se battre, et à quel moment le faire ? Dans les années 1980, les scientifiques pensaient avoir trouvé la réponse. Ils avaient découvert que, lorsque de nouveaux lymphocytes T sont créés dans notre thymus (un petit organe situé à l’arrière de la partie supérieure du sternum), ceux qui risquent d’attaquer nos propres tissus sont éliminés. Les lymphocytes T survivants sont ensuite relâchés dans notre corps, où ils n’attaquent que les intrus. Ce concept est appelé la « tolérance au soi ».

Mais un jeune scientifique japonais, Shimon Sakaguchi, ne s’est pas satisfait de cette explication. Il a décidé de creuser davantage. Il soupçonnait que des lymphocytes T « auto-agressifs » pouvaient parvenir à s’échapper du thymus et se répandre dans l’organisme. Selon lui, un autre mécanisme existait pour faire face à ce cas de figure et contrôler lesdits lymphocytes T. Ce mécanisme fondamental aurait aussi expliqué la survenue de maladies auto-immunes spontanées chez l’être humain.

Il s’avère que Sakaguchi avait raison. En début de semaine, il a été l’un des trois scientifiques récompensés par le prix Nobel de médecine ou physiologie 2025 pour leur découverte des lymphocytes T régulateurs, appelés Treglymphocytes Treg.

Ces cellules immunitaires d’un type particulier sont en quelque sorte des gardes du corps de l’organisme ; leur rôle est d’aider à maintenir le système immunitaire en équilibre. Désormais, ces recherches alimentent des essais cliniques destinés à mettre au point des traitements pour lutter contre le cancer, le diabète, ou pour prévenir le rejet de greffes d’organes.

Je suis Gemma Ware, de The Conversation, un site d’actualité et d’analyse indépendant qui associe journalistes et universitaires. Bienvenue dans The Conversation Weekly, le podcast où des experts vous expliquent comment nous en sommes arrivés là.

TC : Shimon Sakaguchi, vous êtes professeur émérite à l’Immunology Frontier Research Centre de l’université d’Osaka au Japon et corécipiendaire du prix Nobel de physiologie ou médecine de cette année. Félicitations et bienvenue à The Conversation.

SS : Merci beaucoup.

TC : Je crois comprendre que vous étiez dans votre laboratoire lorsque vous avez reçu l’appel vous annonçant que vous aviez remporté le prix. Comment se sont passés les jours qui ont suivi ?

SK : C’était une merveilleuse surprise. J’ai ensuite reçu énormément de messages de félicitations du monde entier. C’est vraiment incroyable, et enthousiasmant.

TC : Revenons au début des années 1980. Vous travailliez alors à l’Institut de recherche sur le cancer d’Aichi, à Nagoya, au Japon. Comment en êtes-vous venu à vous intéresser au fonctionnement du système immunitaire ?
SS : J’étais très intéressé par la tolérance immunologique. Le système immunitaire nous protège des microbes qui tentent de nous envahir. Mais d’un autre côté, parfois, il se retourne contre nous et provoque des maladies auto-immunes. Donc le système immunitaire est à la fois bon et mauvais. Le fait qu’il ne s’en prenne pas à nous, c’est ce que l’on appelle la tolérance au soi. Comprendre comment cette tolérance immunitaire est établie et maintenue, constitue un des thèmes clés de la recherche en immunologie.

TC : Vous vous intéressiez à une expérience menée auparavant par certains de vos collègues sur des souris nouveau-nées. Ils avaient retiré le thymus de ces souris trois jours après leur naissance. Comme le thymus est essentiel au développement de la tolérance immunitaire (c’est d’ailleurs de là que vient le nom des « lymphocytes T », le T étant pour « thymus »), ils pensaient qu’elles auraient un système immunitaire affaibli. Mais en réalité, ce qui s’est produit, c’est que leur système immunitaire s’est emballé et que les souris ont développé des maladies auto-immunes. Qu’est-ce qui vous intriguait tant dans cette expérience ?

SS : L’expérimentation qu’ils ont menée était très intéressante. En effet, si vous enlevez le thymus de souris normales pendant la période néonatale, vous vous attendriez à ce qu’elles présentent une déficience immunitaire puisqu’elles n’ont alors plus de lymphocytes. Mais il s’est passé tout le contraire : elles ont développé des maladies auto-immunes. Des maladies très similaires à celles que l’on observe chez l’être humain. Il se passait donc là quelque chose d’intéressant. Évidemment, chez les patients humains [qui développent des maladies auto-immunes], le thymus n’a pas été retiré. Il devait donc exister un mécanisme commun capable d’expliquer [le résultat observé chez les souris ayant subi une ablation du thymus] et les maladies auto-immunes spontanées chez l’humain.

TC : Vous avez alors décidé d’une autre approche, pour voir si vous pouviez empêcher le système immunitaire des souris sans thymus de s’emballer. Vous avez prélevé des lymphocytes T sur des souris génétiquement identiques et les avez introduits dans l’organisme de celles auxquelles on avait enlevé le thymus. Qu’avez-vous découvert ?

**SS : **C’est tout à fait cela, et de cette façon, la survenue de maladies a pu être prévenue. Cela suggérait donc qu’il devait exister une population de lymphocytes T capable d’empêcher le développement des maladies [auto-immunes]. Une sorte de population « suppressive ».

TC : Racontez-nous ce moment où vous avez réalisé que les souris allaient bien et que vous aviez réussi à les protéger des maladies auto-immunes. Qu’avez-vous ressenti ?

SS : De l’excitation, et le sentiment qu’il s’agissait de quelque chose d’important. Puis que si nous analysions plus en profondeur ce phénomène, il pourrait peut-être nous apprendre un principe immunologique fondamental à propos de la tolérance. Je me disais que si je pouvais découvrir cela, disons, dans les dix ans, ce serait formidable. C’est là tout ce que j’espérais à cette époque.

TC : Aviez-vous conscience à ce moment-là d’avoir fait une grande découverte ?

SS : Une grande découverte ? Disons que dans le domaine de l’immunologie, c’était certainement quelque chose, car c’était essentiel pour comprendre les maladies immunologiques. Quant à savoir si c’était une « grande découverte » ou non… Cela allait dépendre de notre capacité à démontrer que nous pouvions guérir de telles maladies ou en empêcher le développement. À cette époque, il restait encore à savoir comment nous allions pouvoir généraliser ce que nous avions trouvé.

TC : Avez-vous rencontré des difficultés, dans les années 1980, pour poursuivre ces travaux de recherche ?

SS : Il n’a pas été facile d’obtenir des financements, car la communauté des spécialistes en immunologie était très sceptique quant à l’existence de tels lymphocytes. Mais à cette période, j’ai passé près de dix ans aux États-Unis, où j’ai eu beaucoup de chance, car une fondation privée, la Lucille P. Markey Foundation, a soutenu mes recherches pendant huit ans. Le soutien de jeunes chercheurs par des fondations privées était bien plus courant aux États-Unis qu’au Japon. J’espère que ce type de pratique ou de système se poursuivra, non seulement aux États-Unis, mais aussi au Japon.

TC : Vous aviez donc mené cette expérience sur des souris et réalisé qu’il existait un type particulier de lymphocyte T. Mais comprendre plus précisément de quoi il retournait vous a pris environ une décennie. Une fois que vous y êtes parvenu, vous avez baptisé ces lymphocytes T des lymphocytes T régulateurs, ou lymphocytes Treg. Il s’agit donc d’un type particulier de lymphocytes T, qui empêchent notre système immunitaire de surréagir et d’attaquer notre corps. Vous avez publié votre article sur les lymphocytes T régulateurs en 1995. Comment a-t-il été reçu à l’époque ?

SS : Avant cette date, les gens considéraient qu’il s’agissait d’un phénomène intéressant. Mais ce n’est que lorsque nous sommes parvenus à définir cette population grâce à un marqueur spécifique que tout le monde a pu observer les mêmes cellules que nous. Avant cela, les autres chercheurs ne pouvaient pas vérifier que ce que nous affirmions était vrai. Nous avons démontré que ces lymphocytes étaient exprimés fortement, et de façon constitutive. Chacun a ensuite pu reproduire nos expériences et le confirmer.

TC : En gros, ces lymphocytes T régulateurs que vous aviez identifiés circulent et empêchent tout lymphocyte T agressif qui se serait échappé du thymus d’attaquer notre corps. Si nous n’en possédons pas, nous risquons de développer une maladie auto-immune. Mais aujourd’hui, nous savons aussi que le rôle joué par les lymphocytes Treg est beaucoup plus large que cela. Pourquoi est-ce si important ?

SS : J’avais un intérêt pour les maladies auto-immunes, et leurs origines. C’était ce qui motivait mes recherches, ce qui en constituait la force directrice. Mais au fil de mes travaux, j’ai compris que les lymphocytes Treg étaient importants non seulement en matière de maladies auto-immunes, mais aussi pour l’immunité tumorale, la tolérance vis-à-vis des greffons, et plus récemment, la réparation des tissus. Ils ont donc de multiples fonctions. Tout ça est aujourd’hui très enthousiasmant.

TC : Revenons à l’époque où vous identifiiez ces lymphocytes T régulateurs. Vos collègues et corécipiendaires du Nobel, Mary Bruncko et Fred Ramsdell, travaillaient aux États-Unis à comprendre les gènes derrière une maladie auto-immune rare et invalidante. Dans le cadre de ces travaux, ils ont découvert le gène qui contrôle le fonctionnement des lymphocytes T régulateurs. Vous souvenez-vous de la publication de leur article en 2001 ? Quelle a été votre réaction ?

SS : Nous avions remarqué cet article. Un gène avait été identifié et une anomalie ou mutation de ce gène provoquait non seulement des maladies auto-immunes, mais aussi des allergies et des maladies inflammatoires chroniques de l’intestin. Donc un seul gène était responsable de multiples pathologies immunologiques. Ledit gène avait été découvert, mais les auteurs n’avaient pas montré comment cette anomalie génétique entraînait ces maladies immunologiques.

Nous avons immédiatement commencé nos recherches sur ce gène, appelé FoxP3. Nous avons postulé que ce gène devait être lié à la fonction ou au développement des Treg. Nous avons donc commencé diverses expérimentations, et publié nos résultats deux ans plus tard : nous avons démontré que ce gène était spécifique des lymphocytes T régulateurs.

TC : Les connaissiez-vous personnellement ? Étiez-vous en contact avec eux, scientifiquement parlant ?

SS : Non, je ne les connaissais pas à l’époque. Mais bien sûr, nous nous sommes rencontrés lors de congrès scientifiques, en particulier Fred Ramsdell. Ils avaient publié leurs découvertes et les présentaient également dans des colloques.

TC : Nous commençons seulement à comprendre ce que vos découvertes pourraient apporter en matière d’amélioration de la santé. Quelles sont, selon vous, les pistes de recherche les plus prometteuses et sur quoi travaillez-vous actuellement ?

SS : Les Treg sont spécialisées dans la suppression immunitaire. Cela signifie qu’en les renforçant ou en les multipliant, elles pourraient être utilisées pour traiter des maladies immunologiques, notamment les maladies auto-immunes, les allergies ou le syndrome de l’intestin irritable.

Ce qui est enthousiasmant, c’est que plus de 200 essais cliniques sont en cours : on prélève chez les patients des Treg naturellement présents dans leur organisme, on les multiplie puis et on les leur réinjecte.

Mais nous menons aussi des projets plus ambitieux : nous essayons de convertir des lymphocytes T effecteurs ou mémoires spécifiques d’une maladie — donc des « mauvais » lymphocytes — en Treg. Nous espérons de cette façon aboutir à une suppression spécifique d’un antigène ou d’une maladie (le terme « antigène » désigne tout élément étranger à l’organisme capable de déclencher une réponse immunitaire, ndlr).

TC : Ces « mauvais » lymphocytes T qui attaquent l’organisme, vous voulez les transformer en Treg pour qu’ils deviennent des gardes du corps ?
SS : Exactement. C’est ce que nous poursuivons actuellement.

TC : Quelles maladies ciblez-vous ?

SS : Diverses maladies auto-immunes, par exemple des maladies auto-immunes du foie, dont l’hépatite auto-immune, pour laquelle le seul traitement actuellement disponible est la corticothérapie (traitement par corticostéroïdes).

TC : D’autres équipes s’intéressent aussi au cancer. Pouvez-vous expliquer comment cela fonctionnerait ?

SS : C’est un autre espoir en matière de recherche sur les lymphocytes Treg. Ces derniers sont abondants et très fortement activés dans les tissus cancéreux. La réponse immunitaire dirigée contre les cellules cancéreuses est de ce fait inhibée.

L’idée est de trouver une façon de réduire la quantité de Treg et ainsi améliorer la réponse immunitaire antitumorale. Nous espérons à terme parvenir à développer une petite molécule administrable par voie orale qui serait capable de renforcer ladite réponse en faisant diminuer le nombre de lymphocytes Treg présents dans les tissus tumoraux. Nous sommes encore loin de l’objectif, mais ce type de recherche nous intéresse au plus haut point.

TC : En lisant vos travaux, on se rend compte à quel point ils s’appuient sur les recherches de ceux qui vous ont précédé, non seulement au sein de votre propre laboratoire, mais aussi ceux qui ont œuvré durant les décennies précédentes, et qui pour certains ont aussi obtenu un prix Nobel. Qu’aimeriez-vous que l’on fasse de vos découvertes à l’avenir ?

SS : Eh bien, mon espoir immédiat est que les Treg deviennent un outil efficace pour traiter diverses maladies immunologiques, ou que l’on parvienne à les cibler dans le cadre d’immunothérapies anticancéreuses. J’espère que cela deviendra très prochainement une réalité clinique. Dans le même temps, des recherches récentes ont montré que ces lymphocytes ont aussi d’autres fonctions, en plus de leur rôle immunosuppresseur.

Concrètement, cela signifie qu’ils pourraient présenter un intérêt au-delà des maladies immunologiques, notamment dans le traitement de maladies neurodégénératives telles que les maladies d’Alzheimer ou de Parkinson, dans lesquelles l’inflammation joue un rôle. En ciblant cette inflammation, nous pourrions peut-être ralentir leur progression.

C’est une piste très intéressante, nous espérons qu’elle se confirmera, et que cette approche pourra fonctionner pour ce type de pathologies.

The Conversation

Shimon Sakaguchi est le fondateur scientifique et directeur de RegCell, une start-up japonaise qui travaille sur des traitements basés sur les lymphocytes T régulateurs. Il est également conseiller scientifique pour la société de biotechnologie Coya Therapeutics. Il a reçu des financements de l’Agence japonaise pour la recherche et le développement médicaux, de la Société japonaise pour la promotion de la science et pour des recherches collaboratives avec CHUGAI PHARMACEUTICAL, Otsuka Pharmaceutical et RegCell.

ref. Entretien avec Simon Sakaguchi, prix Nobel de médecine – https://theconversation.com/entretien-avec-simon-sakaguchi-prix-nobel-de-medecine-267233

Political violence: What can happen when First Amendment free speech meets Second Amendment gun rights

Source: The Conversation – USA – By Gregory P. Magarian, Thomas and Karole Green Professor of Law, Washington University in St. Louis

The proliferation of guns in the U.S. can elevate political rhetoric to political violence. Douglas Sacha, Moment/Getty Images

The assassination in September 2025 of conservative activist Charlie Kirk has heightened attention on the relationship between political rhetoric and political violence.

Even before police had identified a suspect, President Donald Trump blamed the shooting on the “rhetoric” of the “radical left.” The Trump administration has since acted to silence left-leaning speakers and is threatening to intensify its attacks on left-wing political speech.

But my decades of studying free speech law have convinced me that suppressing political rhetoric, even through social norms rather than law, undermines the discussion, debate and constructive disagreement essential for a healthy democracy.

Gun proliferation complicates the problem by making political violence much easier to carry out.

Rise of political violence

Political violence – by which I mean any physical attack on people that aims to achieve a political goal – harms democracy by shifting the field of political disagreement from debate to aggression.

Under the U.S. constitutional system of limited government and individual rights, political violence by the government – for example, government assaults on anti-government protesters – is among the gravest threats to liberty.

But political violence committed by private individuals or groups also corrodes constitutional democracy. In the United States, acts of private political violence against members of government and against ordinary people have both increased dramatically in recent years.

Political assassinations are the most vivid form of political violence. The Kirk assassination is only the latest example.

An attendee wears a gun on their hip during a candlelight vigil and prayer event at which an American flag is displayed.
An attendee at a candlelight vigil and prayer event for assassinated Turning Point USA Founder Charlie Kirk on Sept. 10, 2025, in Seattle.
David Ryder/Getty Images

In June 2025, a shooter with a “hit list” of left-liberal targets assassinated Minnesota Democratic Rep. Melissa Hortman and her husband. In December 2024, a shooter angry about health insurance costs killed United Healthcare CEO Brian Thompson. In July 2024, a shooter wounded Trump at a campaign rally in a failed assassination attempt.

Political violence also includes bias-motivated murders. In 2022, a white supremacist murdered 10 Black patrons at a grocery store in Buffalo, N.Y. In 2019, an anti-immigrant racist murdered 23 mostly Latino shoppers at a Wal-Mart in El Paso, Texas. In 2018, an antisemite murdered 11 congregants at a Pittsburgh synagogue.

In those incidents and numerous others, extreme political ideas appear to have motivated the attackers. The linkage of extremist speech to lethal violence has prompted calls to legally restrict or punish extremist speech.

Political violence, free speech and cultural editing

The First Amendment, however, protects extremist speech, including advocacy of violence. Violent rhetoric must actually incite or threaten violence to lose the First Amendment’s shelter.

If law cannot curb the sorts of speech that may inspire political violence, what about social norms – widely shared beliefs about what speech is socially acceptable or appropriate?

Much speech that the First Amendment protects from government regulation eventually disappears from public discourse. That happens through a process I call “cultural editing”: popular and institutional rejection of outmoded or repellent ideas. For example, no serious medical conference discusses treating hay fever with cocaine, and no respectable political science panel includes Nazis.

In a social media post after Charlie Kirk’s killing, President Donald Trump blamed ‘radical left’ rhetoric for political violence.

The Trump administration’s blaming of the Kirk assassination on “radical left” rhetoric points toward a deeper level of cultural editing.

Trump and other conservatives have not cited speech that advocated violence against Kirk. Instead, some conservative activists, spurred on by Trump administration officials, called for harassing and punishing critics of Kirk’s statements and actions.

But such criticisms of Kirk, whatever their merits or lack thereof, fall within the scope of ordinary political debate.

Kirk was not a government official, but he had strong influence in the Trump administration. Robust democratic discourse requires space for people to criticize such powerful figures. Large-scale cultural editing of those criticisms, amounting to suppression of left-leaning views, would hurt the public’s ability to discuss and resolve political disagreements.

However, Trump and others who push for suppressing harsh political rhetoric might argue that the stakes of verbal attacks have increased. They might say that U.S. political culture can no longer indulge political invective because political violence has become more common.

Political violence and guns

That argument for suppressing harsh political speech ignores an independent cause of political violence: gun proliferation.

Most political violence in the U.S. involves guns. Guns make political violence easier by erasing the distance between extremist ideas and lethal action. Hate or fanaticism can end a life in an instant, hundreds of yards from the victim.

The U.S. has by far the highest number of civilian guns and rate of civilian gun ownership in the world. Since 2008, when the Supreme Court declared an individual Second Amendment right to keep and bear arms, annual U.S. gun purchases have increased from about 9 million to about 16 million.

Governments often find regulating speech easier, even though less effective, than tackling underlying problems. At times, federal and state governments have addressed political violence by regulating guns. The 1994 federal assault weapons ban exemplifies regulatory efforts to curb overall gun violence.

But the Supreme Court’s Second Amendment cases now appear to bar strong gun regulations.

People in a democratic society need freedom to make harsh, even extreme political statements with a minimum of cultural editing. The Second Amendment protects access to lethal weapons. This combination of free speech and gun rights makes the growing problem of political violence much harder to solve.

The Conversation

Gregory P. Magarian does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

ref. Political violence: What can happen when First Amendment free speech meets Second Amendment gun rights – https://theconversation.com/political-violence-what-can-happen-when-first-amendment-free-speech-meets-second-amendment-gun-rights-265223

Friendships aren’t just about keeping score – new psychology research looks at why we help our friends when they need it

Source: The Conversation – USA – By Jessica D. Ayers, Assistant Professor of Psychological Science, Boise State University

Friendship isn’t about a running tally of who’s doing more. miodrag ignjatovic/E+ via Getty Images

Despite how natural friendship can feel, people rarely stop to analyze it. How do you know when someone will make a good friend? When is it time to move on from a friendship? Oftentimes, people rely on gut intuitions to answer these kinds of questions.

In psychology research, there’s no universally accepted definition of a friend. Traditionally, when psychologists have analyzed friendship, it’s often been through the lens of exchange. How much did that friend do for me? How much did I do for them? The idea is that friendships are transactional, where friends stick around only as long as they are getting at least as much as they are giving in the friendship.

But this focus doesn’t capture what feels like the essence of friendship for many people. We and our colleagues think another model for relationships – what we call risk-pooling – better matches what many people experience. In this kind of friendship, no one is keeping track of who did what for whom.

Our research over the past decade suggests that this kind of friendship was essential for our ancient ancestors to survive the challenges they encountered. And we feel it’s essential for surviving the challenges of life today, whether navigating personal struggles or dealing with natural disasters.

three men drink wine at cafe table with bill on it
Social exchange theory focuses on whether friends are investing and getting the same amount from the relationship.
tim scott/Moment via Getty Images

A focus on what friends give you

The traditional social exchange theory of friendship views relationships as transactions where people keep a tally of costs and benefits. Building on this framework, researchers have suggested that you approach each friendship with a running list of pluses and minuses to decide whether to maintain the bond. You keep friendships that provide more benefits than costs, and you end those that don’t.

The theory holds that this balancing act comes into play when making decisions about what kinds of friendships to pursue and how to treat your friends. It’s even made its way into pop psychology self-help spaces.

We contend that the biggest issue with social exchange theory is that it misses the nuances of real-life relationships. Frankly, the theory’s wrong: People often don’t use this cost-to-benefit ratio in their friendships.

Less accounting, more supporting

Anybody who has seen a friend through tough times – or been the one who was supported – can tell you that keeping track of what a friend does for you isn’t what friendships are about. Friendships are more about companionship, enjoyment and bonding. Sometimes, friendship is about helping just because your friend is in need and you care about their well-being.

Social exchange theory would suggest that you’d be better off dropping someone who is going through cancer treatment or a death in the family because they’re not providing as many benefits to you as they could. But real-life experiences with these situations suggest the opposite: These are the times when many people are most likely to support their friends.

Our research is consistent with this intuition about the shortcomings of social exchange theory. When we surveyed people about what they want in a friend, they didn’t place a high value on having a friend who is conscientious about paying back any debts – something highly valued from a social exchange perspective.

People considered other traits – such as loyalty, reliability, respectfulness and being there in times of need – to be much more important. These qualities that relate to emotional commitment were seen as necessities, while paying back was seen as a luxury that mattered only once the emotional commitment was met.

Having friends who will help you when you’re struggling, work with you in the friendship and provide emotional support all ranked higher in importance than having a friend who pays you back. While they might not always be able to provide tangible benefits, friends can show they care in many other ways.

Of course, friendship isn’t always positive. Some friends can take advantage by asking too much or neglecting responsibilities they could handle themselves. In those cases, it can be useful to step back and weigh the costs and benefits.

Friendship is more than the sum of its parts

But how do friendships actually help people survive? That is one question that we investigated as part of The Human Generosity Project, a cross-disciplinary research collaboration.

The risk-pooling rather than exchange pattern of friendship is something that we found across societies, from “kere kere” in Fiji to “tomor marang” among the Ik in Uganda. People help their friends in times of need without expecting to be paid back.

Two Maasai herders in traditional clothing with herd of cattle against dusty landscape
Maasai people cultivate lifelong relationships called osotua partnerships.
calm_eyes/iStock via Getty Images Plus

The Maasai, an Indigenous group in Kenya and Tanzania who rely on cattle herds to make their living, cultivate friends who help them when they are in need, with no expectation about paying each other back. People ask for help from these special friends, called osotua partners, only when they are in genuine need, and they give if they are asked and able.

These partnerships are not about everyday favors – rather, they are about surviving unpredictable, life-altering risks. Osotua relationships are built over a lifetime, passed down across generations and often marked with sacred rituals.

When we modeled how these osotua relationships function over time, we found they help people survive when their environments are volatile and when they ask those most likely to be able to help. These relationships lead to higher rates of survival for both partners compared to those built on keeping track of debts.

These friends act as social insurance systems for each other, helping each other when needs arise because of unpredictable and uncontrollable events.

And we see this in the United States, just as we do in smaller-scale, more remote societies. In one study, we focused on ranchers in southern Arizona and New Mexico embedded in a network of what they call “neighboring.” They don’t expect to be paid back when they help their neighbors with unpredictable challenges such as an accident, injury or illness. We also found this same pattern in an online study of U.S.-based participants.

In contrast, people such as the ranchers we studied are more likely to expect to be paid back for help when needs arise because of more predictable challenges such as branding cattle or paying bills.

Catastrophic insurance, not tit for tat

What all this research suggests is that friendship is less about the exchange of favors and more about being there for each other when unforeseeable disaster strikes. Friendship seems more like an insurance plan designed to kick in when you need it most rather than a system of balanced exchange.

What lets these partnerships endure is not only generosity, but also restraint and responsibility: Maasai expect their osotua partners to take care of themselves when they can and to ask only when help is truly needed. That balance of care, respect and self-management offers a useful model.

In a world of growing uncertainty, cultivating risk-pooling friendships and striving to be a good partner yourself may help you build resilience. Our ancestors survived with the help of this kind of relationship; our future may depend on them too.

The Conversation

Athena Aktipis receives funding from the National Science Foundation. She is the Executive Director of the Cooperative Futures Institute.

Jessica D. Ayers does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

ref. Friendships aren’t just about keeping score – new psychology research looks at why we help our friends when they need it – https://theconversation.com/friendships-arent-just-about-keeping-score-new-psychology-research-looks-at-why-we-help-our-friends-when-they-need-it-258549

Our engineering team is making versatile, tiny sensors from the Nobel-winning ‘metal-organic frameworks’

Source: The Conversation – USA – By Jie Huang, Chair Professor of Electrical and Computer Engineering, Missouri University of Science and Technology

Prof. Jie Huang stands with the MOF-based breathalyzer his lab developed with support from the NIH. Michael Pierce/Missouri S&T

When the 2025 Nobel Prize in Chemistry honored Omar Yaghi – the “father of metal-organic frameworks,” or MOFs – along with Susumu Kitagawa and Richard Robson, it celebrated more than the creation of a new class of crystalline materials. It recognized a revolution quietly reshaping how scientists capture, store and sense molecules. These MOFs could allow for sensor technologies that make workplaces, the environment and human bodies safer.

What are MOFs, and why do they matter?

MOFs are made by linking metal ions – atoms that carry an electrical charge – with organic molecules, the carbon-based building blocks found in most living things. Together they form tiny, sponge-like structures full of microscopic pores. You can imagine them as an atomic-scale scaffold filled with nano-sized rooms, each precisely engineered to host certain molecules like guests.

A diagram of molecules arranged in a cube structure, with empty space in each cube.
Metal-organic frameworks, such as MOF-5 shown here, have metal components, organic ‘linkers’ and a cavity that can allow in gases.
Tony Boehle/Wikimedia Commons, CC BY-SA

Because chemists can mix and match different metals and organic linkers, there are thousands of possible MOFs – each with unique properties. Depending on how they’re structured, some have so much internal surface area that a single gram could cover a football field.

This sponge-like porosity – meaning lots of tiny holes inside – lets MOFs trap and release gases, store energy-rich fuels like hydrogen, and capture harmful pollutants. MOFs can use a variety of chemicals in their structure, which lets researchers fine-tune how strongly an MOF interacts with specific molecules.

These features have already inspired potential uses such as capturing carbon dioxide from the air to reduce greenhouse gas concentrations in the atmosphere, pulling clean water from humid air, and delivering medicines inside the body. Over the past decade, the unique properties of MOFs have also opened new possibilities for sensing and detection.

Since 2016, our team of engineers has been developing MOF-based sensors that can detect certain gases and vapors in an environment in real time. These materials’ unique properties are opening new possibilities for sensing in health, safety and environmental monitoring.

From a storage material to a sensing material

When an MOF takes in gas or liquid molecules, its tiny framework changes ever so slightly: It may change in size, how it bends light, or how it conducts electricity, depending on what and how many molecules it absorbs.

By connecting MOFs to devices that can sense changes in light or electricity, researchers can turn these tiny shifts into measurable signals such as light, frequency or voltage. The signals then reveal what chemical is present and how much of it there is. In simple terms, when molecules enter or leave the MOF’s pores, they slightly change how light travels through it or how electricity behaves around it, and those changes become the sensor’s readable output.

Our group at Missouri University of Science and Technology has developed several kinds of MOF-based sensor platforms. Across all these platforms, the core idea is the same: MOFs act as selective sponges that temporarily hold certain gas molecules in their tiny cages, and our devices measure the timing and amount of this uptake and release.

In one study, we attached a single crystal of a copper-based MOF called HKUST-1 to the smooth, flat end of a cut optical fiber – the same kind of thin glass strand used to carry internet and phone signals.

This crystal-fiber combination worked as a tiny device that could measure how light waves interfere with each other. As nearby gas molecules moved into the tiny pores of the MOF crystal, the way it bent and reflected light changed slightly. The optical fiber – connected to a light source and detector – picked up these changes, allowing us to see in real time how many gas molecules the material was taking in.

Our probes show not just that gas molecules enter the tiny cages of the MOF, but also how fast they come and go. By measuring both the amount and the speed of adsorption and release, we can tell which molecules are being taken up and in what proportion, when several are present together. This dynamic view helps us see, in real time, how the material selects one target gas over others. It turns adsorption into a measurable, useful signal for sensing and identification.

In health care, an MOF can act like a selective sponge for specific breath molecules that indicate real, measurable diseases. For example, an MOF designed to adsorb acetone can capture and concentrate this gas from exhaled breath. Acetone levels rise above normal values in people with diabetic ketoacidosis, allowing the sensor to clearly and quantitatively detect the disease.

A photo showing a tube-like device, and a person exhaling into it out of their nose. A cloud of breath hangs in the air between.
Prof. Jie Huang and his team at Missouri S&T developed an MOF–based breath sensor, funded by the NIH, that was developed for COVID-19 and can also be employed for detecting disease biomarkers such as acetone and ammonia in exhaled breath.
Michael Pierce/Missouri S&T

Likewise, an MOF that selectively adsorbs ammonia can concentrate this compound from exhaled breath. Ammonia levels increase above normal values in people with chronic kidney disease, so the sensor can provide a definite indicator of reduced kidney function. Integrating such MOFs into sensor hardware would allow for sensitive, noninvasive screening for these two diseases, based on quantifiable breath markers.

Coating a material in a thin layer of MOFs can take hours. But recently, we developed a quick and simple “droplet-drying” method that forms a crystal layer of the copper-based MOF HKUST-1 directly onto the end of an optical fiber in under two minutes. The resulting film, only about 1/20th the width of a human hair, acted as a high-performance gas sensor that detected humidity, ethanol or carbon dioxide in the environment within seconds.

We also combined MOFs with a hand-held metal device that can sense changes in microwave signals – a bit like how a radio antenna picks up invisible waves in the air. When gas molecules entered the MOF layer, they slightly changed how the device responded to those waves, allowing it to detect gases with remarkable sensitivity.

This sensor made for a low-cost, portable device that could tell one kind of gas molecule apart from another, rather than just detecting that some gas is present. It’s like having a nose that can tell apples from oranges, not just detect that something smells fruity.

Our research suggests that MOF sensors within compact, energy-efficient devices can pick out specific molecules – even when only trace amounts are present in the air. The pores of an MOF can be designed to concentrate specific target molecules. All molecules smaller than the window to an MOF cage will get into the cage. So, we design the sensors so that the molecules we are interested in sensing will reside in the cages longer. The huge internal surface area created by these pores makes them incredibly responsive. Even just a few trapped molecules can trigger a clear signal.

These sensors also work at room temperature and our research suggests they are more precise and adaptable than many traditional chemical sensors.

Toward real-world impact

The main challenges lie in improving MOFs’ long-term durability and environmental resistance. Many frameworks degrade under humidity or heat, though some research groups are looking into how to make them more stable.

When combined with machine-learning algorithms, these sensors can learn to recognize patterns from several gases at once, rather than detecting just one chemical at a time – much like how a human nose can tell different smells apart. This capability could even extend to human breath monitoring, where subtle changes in exhaled gases provide early clues to diseases such as diabetes, lung infections or cancer.

Researchers are working to embed MOFs into flexible films, printed circuits and wireless devices. With these new advances and further research, MOFs could bridge chemistry and engineering one day. As the Nobel Prize recognized, MOFs exemplify how design at the molecular scale can help mitigate problems humans face at a global scale.

If researchers can scale up this technology and overcome the challenges, networks of fiber-optic and microwave MOF sensors could one day monitor industrial plants, pipelines and even human breath for unwanted chemicals to improve safety, efficiency and health.

The Conversation

Jie Huang receives research funding from the U.S. Army Research Laboratory and the National Institutes of Health.

Rex Gerald receives research funding from the U.S. Army Research Laboratory and the National Institutes of Health.

Bohong Zhang and Chen Zhu do not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and have disclosed no relevant affiliations beyond their academic appointment.

ref. Our engineering team is making versatile, tiny sensors from the Nobel-winning ‘metal-organic frameworks’ – https://theconversation.com/our-engineering-team-is-making-versatile-tiny-sensors-from-the-nobel-winning-metal-organic-frameworks-267103