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Scientists have identified processes that control the development and composition of thymic tissue throughout life. Specifically, they were able to show that a certain growth factor can maintain progenitor cells even in the aging thymus and thus counteract the age-related shrinkage of the organ and the reduction in the number of powerful immune cells. The results provide new avenues for therapeutic approaches to autoimmune diseases.
The thymus is a crucial organ of the immune system. In the thymus, the well-known T cells mature: As killer cells, they recognize and destroy virus-infected or malignant cells, and as so-called helper T cells they assist the body in antibody formation. In the last decades, Thomas Boehm’s research group at the Max Planck Institute of Immunobiology and Epigenetics in Freiburg has identified the genetic switches required for T cell maturation in the thymus. An essential component for this process are so-called thymic epithelial cells, which attract T cell precursors and induce them to mature into fully functional T cells. During this development, T cells are instructed to distinguish diseased from healthy cells and foreign material from the body’s own cells, thus enabling them to detect and eliminate unwanted structures and prevent autoimmune diseases. Earlier work in the Boehm laboratory had shown that the two main types of thymic epithelium arise from bipotent progenitor cells. However, it was unclear whether there is more than one type of progenitor, and it was unknown into how many subforms the progenitors differentiate.
Molecular family tree analysis identifies progenitor cells
In collaboration with the laboratory of Dominic Grün (previously at the MPI of Immunobiology and Epigenetics in Freiburg, now Max Planck Research Group at the University of Würzburg), a specialist in single-cell RNA analysis, the researchers have now succeeded in describing the unexpected diversity of thymic epithelial cells at the transcriptional level. Algorithms developed in Grün’s laboratory for the precise description of differences in the gene activity of individual cells made it possible to identify potential precursor cells. In a second step, the researchers experimentally verified the predictions using a “barcoding” system developed in the laboratory of Thomas Boehm using CRISPR gene editing. The barcoding method allows to assign a molecular signature to precursor cells, which is then carried along by all cells that emerge from the precursors. In this way, the researchers derived a family tree of epithelial cells.
After a long period of method development that was marked by many setbacks, Anja Nusser from the Boehm lab and Sagar from the Grün lab jointly succeeded in developing a method that connects information from the phylogenetic tree with the molecular characteristics of individual cells. As a result, for the first time it became possible to study the development of thymic epithelium at different ages in equisite molecular detail. This kind of analysis is of particular interest to immunologists because the thymus is subject to significant changes during life. Rapid organ growth and massive T-cell production are characteristic of the early developmental stages. In contrast, there is a gradual loss of functional thymic epithelial cells in old age and, therefore, decreased T-cell production. These age-related changes are associated with a reduced immune function.
Successive activities of the progenitor cells determine the composition of the thymus
The researchers identified two bipotent progenitor populations of the thymic epithelium in their analysis. An “early” progenitor population takes over the primary role in the thymus formation during embryonic development. While in the juvenile organism, a subsequent “postnatal” progenitor population significantly determines the continued thymus formation in adulthood. Interestingly, the progenitor populations’ temporal order modulates the thymic epithelium’s composition.
At early time points, mainly cortical thymic epithelial cells are formed, which primarily contribute to the production of T cells. At later time points, the primary output is on medullary thymic epithelial cells. They ensure that no self-reactive T cells are released from the thymus into the body and thus, contribute significantly to protection against autoimmunity. New therapeutic approaches to increase thymic function
The sophisticated combination of transgenic animal models from the Boehm laboratory with state-of-the-art methods of single-cell profiling of the Grün group allowed the researchers to examine the effect of increasing the proliferation of thymic epithelial cells. It was of particular importance to determine whether early stimulation of the thymus with a dedicated growth factor leads to undesirably faster consumption of stem cells and thus to premature shrinkage of the thymus. However, the data obtained by the researchers suggest that this is not the case. “The stimulated thymus of an old mouse is still larger than that of an unstimulated young mouse. Moreover, the fine tissue structure of the stimulated thymus shows the typical structure of cortical zones and medullary areas inside the organ,” says Max Planck director Thomas Boehm. These results lay the foundation for developing new therapeutic approaches to correct age-related thymic shrinkage and treat T-cell-dependent autoimmune diseases.

Immune response and the lymphatic system are central to cardiac repair after a heart attack, according to a study from Ann & Robert H. Lurie Children’s Hospital of Chicago and Northwestern University Feinberg Cardiovascular Research Institute. These insights into the basic mechanisms of cardiac repair are the first step towards developing novel therapeutic approaches to preserve heart function. Findings were published in the Journal of Clinical Investigation.
“We found that macrophages, or immune cells that rush to the heart after a heart attack to ‘eat’ damaged or dead tissue, also induce vascular endothelial growth factor C (VEGFC) that triggers the formation of new lymphatic vessels and promotes healing,” said co-senior author Edward Thorp, PhD, from the Heart Center at Lurie Children’s and Associate Professor of Pathology and Pediatrics at Northwestern University Feinberg School of Medicine. “Our challenge now is to find a way either to administer VEGFC or to coax these macrophages to induce more VEGFC, in order to speed the heart repair process.”
People who suffer a heart attack are at high risk for heart failure, even with the advances in medications to reduce mortality. This occurs in part because some macrophages that arrive at the site of damage are proinflammatory and do not induce VEGFC.
“It is a Dr. Jekyll and Mr. Hyde scenario, with ‘good’ macrophages that induce VEGFC and the ‘bad’ ones that don’t. We need to prevent the ‘bad’ macrophages from causing further damage,” said co-senior author Guillermo Oliver, PhD, Director of Feinberg Cardiovascular and Renal Research Institute — Center for Vascular and Developmental Biology, and Professor of Medicine at Northwestern University Feinberg School of Medicine. “We are working to understand more about the progression to heart failure after a heart attack, in order to intervene early and reset the course to cardiac repair.”
Research at Ann & Robert H. Lurie Children’s Hospital of Chicago is conducted through Stanley Manne Children’s Research Institute. The Manne Research Institute is focused on improving child health, transforming pediatric medicine and ensuring healthier futures through the relentless pursuit of knowledge. Lurie Children’s is ranked as one of the nation’s top children’s hospitals by U.S. News & World Report. It is the pediatric training ground for Northwestern University Feinberg School of Medicine.
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Materials provided by Ann & Robert H. Lurie Children’s Hospital of Chicago. Note: Content may be edited for style and length.

Cilia are the body’s diligent ushers. These microscopic hairs, which move fluid by rhythmic beating, are responsible for pushing cerebrospinal fluid in your brain, clearing the phlegm and dirt from your lungs, and keeping other organs and tissues clean.
A technical marvel, cilia have proved difficult to reproduce in engineering applications, especially at the microscale.
Cornell researchers have now designed a micro-sized artificial cilial system using platinum-based components that can control the movement of fluids at such a scale. The technology could someday enable low-cost, portable diagnostic devices for testing blood samples, manipulating cells or assisting in microfabrication processes.
The group’s paper, “Cilia Metasurfaces for Electronically Programmable Microfluidic Manipulation,” published May 25 in Nature. The lead author is doctoral student Wei Wang.
“There are lots of ways to make artificial cilia that respond to light, magnetic or electrostatic forces,” Wang said. “But we are the first to use our new nano actuator to demonstrate artificial cilia that are individually controlled.”
The project, led by the paper’s senior author, Itai Cohen, professor of physics in the College of Arts and Sciences, builds off a platinum-based, electrically-powered actuator — the part of the device that moves — his group previously created to enable microscopic robots to walk. The mechanics of those bending bot legs is similar, but the cilia system’s function and applications are different, and quite flexible.

DNA mutations are essential to the rapid development of an array of antibody-producing immune cells called B cells that collectively can recognize a vast number of specific targets. But this process can go awry in people with a mutation in a gene called SETD2, leading to a type of aggressive blood cancer, according to a study by Weill Cornell Medicine investigators.
The study, published April 20 in Cancer Discovery, found that having a mutation in one of the two copies of SETD2 in B cells can lead to a proliferation of cells that don’t readily repair their mutated DNA, causing an aggressive type of cancer called diffuse large B cell lymphoma (DLBCL).
“However, when both copies of this gene are mutated in the cancer cell, it is fatal to the cell, suggesting that drugs that target SETD2 might offer an effective treatment option for this type of lymphoma,” said senior author Dr. Ari Melnick, the Gebroe Family Professor of Hematology/Oncology in the Division of Hematology and Clinical Oncology and a member of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine.
Researchers have previously found that the SETD2 mutation disproportionately occurs in DLBCL in people of African ancestry.
“The finding points to a possible therapeutic intervention for these patients, who don’t otherwise have good options,” said Dr. Melnick. The strategy is now being tested in a phase 1 clinical trial.
Diffuse large B cell lymphoma develops in B cells in the lymph nodes of humans, dogs and some other mammals. To understand the underlying causes, lead author Dr. Wilfred Leung examined B cells of mice genetically engineered to lack one copy of SETD2. He began the study as a doctoral candidate in the laboratory of Dr. Kristy Richards, who was an associate professor with a joint appointment at the College of Veterinary Medicine at Cornell University and Weill Cornell Medicine. Her laboratory had studied cancer in humans and canines to accelerate the development of potential new treatments. Dr. Leung joined Dr. Melnick’s laboratory to complete the work after Dr. Richards died of breast cancer in 2019.

Alabama

Gov.

Sen.

House

22 weeks

Prohibited

Weeks or months

A judge blocked a total ban on abortion, with no exceptions for rape or incest, but abortion opponents would most likely seek its enforcement if Roe were overturned.

Arkansas

22 weeks

Prohibited

Immediately

A trigger law banning nearly all abortions, with no exceptions for rape or incest, would take effect within days.

Idaho

Viability

Prohibited

Immediately

A trigger law banning nearly all abortions would take effect 30 days after the Supreme Court’s decision.

Kentucky

22 weeks

Prohibited

Immediately

A trigger law banning nearly all abortions, with no exceptions for rape or incest, would take effect immediately.

Louisiana

22 weeks

Prohibited

Immediately

A trigger law banning nearly all abortions, with no exceptions for rape or incest, would take effect immediately.

Mississippi

20 weeks

Prohibited

Immediately

A trigger law banning nearly all abortions would take effect within days.

Missouri

Viability

Prohibited

Immediately

A trigger law banning nearly all abortions, with no exceptions for rape or incest, would take effect within days.

North Dakota

22 weeks

Prohibited

Immediately

A trigger law banning nearly all abortions would take effect 30 days after the Supreme Court’s decision.

Oklahoma

6 weeks

Prohibited

Immediately

A trigger law banning nearly all abortions, with no exceptions for rape or incest, would take effect within days.

South Dakota

22 weeks

Prohibited

Immediately

A trigger law banning nearly all abortions, with no exceptions for rape or incest, would take effect immediately.

Tennessee

20 weeks

Prohibited

Immediately

A trigger law banning nearly all abortions, with no exceptions for rape or incest, would take effect about 30 days after the court overturned Roe.

Texas

6 weeks

Prohibited

Immediately

A trigger law banning nearly all abortions, with no exceptions for rape or incest, would take effect 30 days after the Supreme Court’s decision.

Utah

Viability

Prohibited

Immediately

A trigger law banning nearly all abortions would take effect within days.

West Virginia

22 weeks

Prohibited

Weeks or months

Voters approved an amendment to the state’s Constitution that denies any right to abortion. Lawmakers could use the amendment to enact a total ban.

Wyoming

Viability

Prohibited

Immediately

A trigger law banning nearly all abortions would take effect within 30 days of the Supreme Court’s decision.

Arizona

Viability

Prohibited or restricted

Weeks or months

The state enacted an abortion ban after 15 weeks, with no exceptions for rape or incest, which should take effect in September. It has an inactive ban from before 1973, but the governor has said the 15-week ban would take precedence.

Florida

24 weeks

Prohibited or restricted

Weeks or months

The state enacted an abortion ban after 15 weeks of pregnancy, which will go into effect in July. The state’s high court recognized the right to abortion in its Constitution three decades ago, but the court has become more conservative, with three of the seven judges appointed by the Republican governor.

Georgia

22 weeks

Prohibited or restricted

Weeks or months

The state enacted a ban on abortion after six weeks of pregnancy, but a court blocked it. The state filed an appeal and a court stayed the case pending a Supreme Court decision on Dobbs.

Ohio

22 weeks

Prohibited or restricted

Weeks or months

The state enacted a ban on abortion after six weeks of pregnancy, with no exceptions for rape or incest, but it is temporarily blocked in court. Abortion opponents are likely to seek its enforcement.

South Carolina

22 weeks

Prohibited or restricted

Weeks or months

The state enacted a ban on abortion after six weeks of pregnancy, but a court blocked it. The state filed an appeal and a court stayed the case pending a Supreme Court decision on Dobbs.

Our brains rarely record single memories — instead, they store memories into groups so that the recollection of one significant memory triggers the recall of others connected by time. As we age, however, our brains gradually lose this ability to link related memories.
Now UCLA researchers have discovered a key molecular mechanism behind memory linking. They’ve also identified a way to restore this brain function in middle-aged mice — and an FDA-approved drug that achieves the same thing.
Published in Nature, the findings suggest a new method for strengthening human memory in middle age and a possible early intervention for dementia.
“Our memories are a huge part of who we are,” explained Alcino Silva, a distinguished professor of neurobiology and psychiatry at the David Geffen School of Medicine at UCLA. “The ability to link related experiences teaches how to stay safe and operate successfully in the world.”
A bit of Biology 101: cells are studded with receptors. To enter a cell, a molecule must latch onto its matching receptor, which operates like a doorknob to provide access inside.
The UCLA team focused on a gene called CCR5 that encodes the CCR5 receptor — the same one that HIV hitches a ride on to infect the brain cell and cause memory loss in AIDS patients.

Some residents of Belmont County in eastern Ohio have long suffered from headaches, fatigue, nausea and burning sensations in their throats and noses. They suspected these symptoms were the result of air pollution from fracking facilities that dominate the area, but regulators dismissed and downplayed their concerns.
With the technical assistance of volunteer scientists at Columbia University’s Lamont-Doherty Earth Observatory, MIT and the American Geophysical Union’s Thriving Earth Exchange, local advocacy groups set up their own network of low-cost sensors. They found that the region’s three EPA sensors were not providing an accurate picture: The sensors revealed concerning levels of air pollution, and correlations between local spikes and health impacts.
The results are published today in the journal Environmental Research Letters.
Nestled in an Appalachian valley, Belmont has been booming with new infrastructure to extract and process natural gas. Fracking is known to emit pollutants including particulate matter and volatile organic compounds such as benzene, toluene and ethylbenzene, which have been linked to respiratory and cardiovascular health problems. Lung and bronchus cancer have become the leading cause of cancer deaths in Ohio. A 2017 Yale Public Health analysis confirmed the need for additional monitoring and regulation for chemicals associated with unconventional oil and gas development.
Concerned about the fumes in certain areas of the community and the lack of information and transparency, two activist groups, Concerned Ohio River Residents and the Freshwater Accountability Project, wanted to set up a high-density monitoring network. After submitting their proposal to the Thriving Earth Exchange, which enables collaborations between community groups and volunteer scientists, they were paired with Garima Raheja, a PhD candidate who studies air pollution at Lamont-Doherty.
“We realized that the Thriving Earth Exchange program would give us valuable aid to validate the complaints we often receive from those living near pollution sources in a way that would provide credible and actionable data to improve air quality in the region,” said Lea Harper, managing director of Freshwater Accountability Project.

Pregnant women and new mothers are often presented with information on the benefits of breastfeeding their infants. A new study in Annals of Allergy, Asthma and Immunology, the scientific journal of the American College of Allergy, Asthma and Immunology (ACAAI) shows that a longer period of exclusive breastfeeding was associated with decreased odds of current asthma.
“The results of the study indicated that the longer a mother exclusively breastfed, the lower the relative odds of her child having asthma, or asthma-related outcomes,” said Keadrea Wilson, MD, lead author of the study and Assistant Professor of Neonatology at the University of Tennessee Health Science Center. “There was a ‘dose-response’ effect depending on how long the mother breastfed: Babies that were breastfed for 2-4 months had only 64% likelihood of having as many asthma outcomes as those who were breastfed less than 2 months; those breastfed for 5-6 months had 61% likelihood, and those breastfed for more than 6 months had a 52% likelihood.”
The study combined three studies to get a large number of subjects — more than 2,000 mother-child pairs. In addition, by combining the studies, the authors achieved a demographic distribution. For example, 38% of the respondents were Black and 6% were Hispanic/Latina.
“A further finding of the study was that duration of breastfeeding mixed with formula/juices/other foods (so not exclusively breastfed) did not provide the same level of protection,” says allergist Angela Hogan, MD, vice chair of the ACAAI Asthma Committee. Dr. Hogan was not involved in the research. “Asthma runs in families, and according to the CDC, if a child has a parent with asthma, they are three to six times more likely to develop this condition than someone who does not have a parent with asthma. Anything a parent can do to lower the odds of their child getting asthma is worth considering.”
“Our study strengthens current breastfeeding recommendations which reflect recent analysis that show lower risk of asthma with more versus less breastfeeding,” said Dr. Wilson.
Allergists are specially trained to test for, diagnose and treat asthma. To find an allergist near you who can help create a personal plan to deal with your or your child’s asthma, and help them live their best life, use the ACAAI allergist locator.
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Materials provided by American College of Allergy, Asthma, and Immunology. Note: Content may be edited for style and length.

When something goes wrong in mitochondria, the tiny organelles that power cells, it can cause a bewildering variety of symptoms such as poor growth, fatigue and weakness, seizures, developmental and cognitive disabilities, and vision problems. The culprit could be a defect in any of the 1,300 or so proteins that make up mitochondria, but scientists have very little idea what many of those proteins do, making it difficult to identify the faulty protein and treat the condition.
Researchers at Washington University School of Medicine in St. Louis and the University of Wisconsin-Madison systematically analyzed dozens of mitochondrial proteins of unknown function and suggested functions for many of them. Using these data as a starting point, they identified the genetic causes of three mitochondrial diseases and proposed another 20 possibilities for further investigation. The findings, published May 25 in Nature, indicate that understanding how mitochondria’s hundreds of proteins work together to generate power and perform the organelles’ other functions could be a promising path to finding better ways to diagnose and treat such conditions.
“We have a parts list for mitochondria, but we don’t know what many of the parts do,” said co-senior author David J. Pagliarini, PhD, the Hugo F. and Ina C. Urbauer Professor and a BJC Investigator at Washington University. “It’s similar to if you had a problem with your car, and you brought it to a mechanic, and upon opening the hood they said, ‘We’ve never seen half of these parts before.’ They wouldn’t know how to fix it. This study is an attempt to define the functions of as many of those mitochondrial parts as we can so we have a better understanding of what happens when they don’t work and, ultimately, a better chance at devising therapeutics to rectify those problems.”
Mitochondrial diseases are a group of rare genetic conditions that collectively affect one in every 4,300 people. Since mitochondria provide energy for almost all cells, people with defects in their mitochondria can have symptoms in any part of the body, although the symptoms tend to be most pronounced in the tissues that require the most energy, such as the heart, brain and muscles.
To better understand how mitochondria work, Pagliarini teamed up with colleagues, including co-senior author Joshua J. Coon, PhD, a UW-Madison professor of biomolecular chemistry & chemistry and an investigator with the Morgridge Institute for Research; and co-first authors Jarred W. Rensvold, PhD, a former staff scientist in Pagliarini’s lab, and Evgenia Shishkova, PhD, a staff scientist in Coon’s lab, to identify the functions of as many mitochondrial proteins as possible.
The researchers used CRISPR-Cas9 technology to remove individual genes from a human cell line. The procedure created a set of related cell lines, each derived from the same original cell line but with a single gene deleted. The missing genes coded for 50 mitochondrial proteins of unknown function and 66 mitochondrial proteins with known functions.

Australian researchers have discovered the key immunological changes that support the remission of peanut allergy in children, paving the way for new, more targeted treatments.
The research showed for the first-time specific gene networks are rewired to drive the transition from peanut allergy to clinical remission following a combination treatment of a probiotic and peanut oral immunotherapy.
Led by the Murdoch Children’s Research Institute (MCRI) and the Telethon Kids Institute, and published in Allergy, the study found that this network reprogramming essentially shuts down the allergic immune response that was responsible for causing a food allergy.
Lead researcher, Murdoch Children’s Professor Mimi Tang, said this was the first study to map the complex gene to gene communication and connectivity underlying clinical remission of peanut allergy.
“The immunological changes leading to remission of peanut allergy were largely unknown,” she said. Previous studies had mostly focused on examining the levels of gene expression, without also exploring how genes interact with each other. But genes don’t work in isolation; instead, biological responses are controlled by large numbers of genes communicating with each other, so it made sense to look at these interactions more closely.
“What we found was profound differences in network connectivity patterns between children who were allergic and those who were in remission. These same changes were also seen when we compared gene networks before and after immunotherapy in the children who achieved remission following immunotherapy.”
The randomised controlled trial involved 62 peanut allergic children from Melbourne, aged 1-10 years, who received a combination treatment of a probiotic and oral immunotherapy (the gradual introduction of the allergenic food) or a placebo. Following 18 months of treatment, 74 per cent taking the combination treatment achieved remission compared with 4 per cent in the placebo group.