Scanning electron microscope image of T regulatory cells (red) interacting with antigen-presenting cells (blue). T regulatory cells can suppress responses by T cells to maintain homeostasis in the immune system. Credit: National Institute of Allergy and Infectious Diseases/NIH
Cedars-Sinai Health Sciences University investigators have identified for the first time a protein’s role as a “dimmer switch” that can calm an overactive immune system and restrain harmful inflammation. The protein, Butyrophilin 2A2 (BTN2A2), interacts with a key molecule that controls the strength of T-cell responses.
The findings, published inNature Communications, define a unique pathway that helps balance immune activity and could be harnessed to limit damage caused by a variety of autoimmune diseases.
In laboratory mice, loss of BTN2A2 led to exaggerated immune reactions and an increase in damaging kidney inflammation called glomerulonephritis. Treatment with BTN2A2 reduced disease severity by increasing immune-regulating T cells and lowering inflammation.
Supporting laboratory experiments in human T-cells demonstrated similar immune-calming effects.
“Glomerulonephritis remains a leading cause of chronic kidney disease and kidney failure worldwide, with limited treatment options,” said Ananth Karumanchi, MD, co-corresponding author of the study and director of the Renovascular Research Center at Cedars-Sinai. “Our findings provide a strong foundation for future studies aimed at modifying immune-driven kidney disease rather than simply managing its symptoms. The pathway could also be targeted in a range of autoimmune and inflammatory diseases including rheumatoid arthritis, multiple sclerosis, inflammatory bowel disease, and transplant rejections.”
Other Cedars-Sinai authors include Shafat Ali, Anders H. Berg, Michifumi Yamashita, Ambart E. Covarrubias, Jordan Mundell, Pranali N. Shah, Ruan Zhang, Vincent Dupont, Bong-Ha Shin, Shen Yang, Madhusudhanarao Katiki, Ramachandran Murali, Margareta D. Pisarska, Ravi Thadhani, Peter S. Heeger and Stanley C. Jordan
An analysis of biomarkers in patient blood samples could help with early detection of cachexia, or cancer wasting syndrome, according to new research published in Cancers. The study by Cedars-Sinai Health Sciences University investigators, explores biologic signals detectable in the blood that could be used to design future strategies for assessing patient risk and developing therapies aimed at mitigating fatigue and muscle and fat loss experienced by many patients with cancer.
“We found that in patients with advanced non-small cell lung cancer, cachexia biomarkers change over time,” said Kamya Sankar, MD, co-medical director of the Thoracic Disease Research Group at Cedars-Sinai Cancer and corresponding author of the study. “And treatments targeting one of the early cachexia biomarkers we identified, an inflammatory protein called GDF-15, are already under evaluation in clinical trials.”
Investigators measured the blood of 27 patients with non-small cell lung cancer at two different time points. In patients with early cachexia, they found higher levels of inflammatory proteins such as GDF-15. In patients with later-stage cachexia, they found increased mitochondrial DNA, which comes from the parts of cells that convert food into energy.
Larger, prospective studies are required to validate the clinical benefit of these biomarkers, but they could serve as the basis for risk assessment of patients and may inform design of future clinical trials of therapies for cancer-associated cachexia, Sankar said.
Additional Cedars-Sinai authors include Elham Kazemian, Nicole Lorona, Carlos D. Cruz-Hernández, Mitra Mastali, Akil A. Merchant, Jennifer Van Eyk, Karen L. Reckamp, Neil A. Bhowmick, and Jane C. Figueiredo.
Other authors include Alex K. Bryant and Puneeth Iyenga
Biologics may be more effective with earlier treatment initiation, especially among children with early polysensitisation or multiple early-childhood risk factors, according to the results of a new study published in Annals of the American Thoracic Society. Screening for these risk factors may help inform targeted early initiation of biologics for asthma.
Robust real-world data on the effectiveness of biologic therapies in children with severe asthma remain limited, particularly across different ages and early-life risk profiles. This evidence gap constrains precision in treatment decisions and clinical guidance.
Children with moderate to severe asthma requiring biologic therapy are most affected, especially those initiating biologic treatment at younger ages and those with early indicators of allergic disease or high-risk asthma histories.
Initiating biologic therapy earlier in childhood – particularly in children with significant early-life risk factors and allergic sensitisation – is associated with greater reductions in severe asthma exacerbations in real-world practice.
Findings highlight the importance of treatment timing and patient history when optimizing outcomes with asthma biologics.
Risks of delayed treatment initiation
Delayed initiation of biologic therapy until adolescence or failure to account for early-childhood risk profiles may reduce potential treatment benefit. These findings highlight the risk of suboptimal outcomes when treatment timing or patient selection does not align with underlying disease risk.
Clinicians should prioritise earlier identification and risk-stratified initiation of biologics in children with severe asthma, particularly those with high early-life risk burden, to maximise treatment benefits.
Study findings support development of care pathways that incorporate earlier, risk-stratified biologic initiation. Decision-making algorithms may benefit from integrating age at treatment initiation and early-life risk indicators, such as polysensitisation and high early disease burden, to better identify children most likely to benefit and reduce severe exacerbations.
Future research may also explore the role of clinical artificial intelligence in supporting these approaches. Clinical AI tools could help identify high-risk paediatric patients earlier and guide treatment timing and patient selection by detecting patterns in real-world clinical data, potentially improving precision in biologic therapy use.
People who use drugs with anticholinergic effects, including certain antidepressants, drugs for urinary incontinence and common antihistamines, are at higher risk of developing cardiovascular disease. This is shown in a new study from Karolinska Institutet published in BMC Medicine.
Anticholinergic drugs reduce the effect of the neurotransmitter acetylcholine and are commonly prescribed to middle-aged and older people. This large group of drugs includes antihistamines used for allergic conditions, anxiety or insomnia, drugs for urinary incontinence, and certain antidepressants, where tricyclic antidepressants have a strong anticholinergic effect, whereas SSRIs have a weaker effect. A high cumulative use of these drugs, referred to as anticholinergic burden (see fact box), has previously been linked to impaired cognitive ability.
May affect heart regulation
The new study suggests that the drugs may also affect the parasympathetic nervous system and thereby the regulation of the cardiovascular system. The results show that it may be important to monitor the total drug burden in everyday clinical practice.
The study included more than 500 000 people in Stockholm who were 45 years of age or older and had no prior cardiovascular disease, except for hypertension, at the start of the study. The researchers followed the participants for up to 14 years and analysed how the use of anticholinergic drugs was associated with the development of cardiovascular disease.
“Many of these drugs are used by older people and by people with multiple medical conditions. We wanted to investigate whether the total exposure had any significance for the risk of developing cardiovascular disease over time,” says Nanbo Zhu, postdoctoral researcher at the Department of Neurobiology, Care Sciences and Society, Karolinska Institutet.
71 per cent higher cardiac risk
The study showed that the risk of cardiovascular disease increased in line with how much anticholinergic medication the participants used each year. Those with the highest exposure had a 71% higher risk of a cardiovascular event than people who did not use anticholinergic medication at all. The association was seen for all types of cardiovascular disease but was particularly clear for heart failure and various forms of arrhythmia.
“Our results indicate that the cumulative drug burden can affect heart regulation, not only in the short term but also over the long term. This does not mean that the drugs should always be avoided, but that exposure should be monitored carefully,” says Hong Xu, assistant professor at the Department of Neurobiology, Care Sciences and Society.
The researchers point out that the study is observational, meaning it cannot establish a causal relationship. Other factors, such as underlying diseases, may also influence the associations.
The work was carried out within the Stockholm CREAtinine Measurements project in collaboration between several research groups at Karolinska Institutet and Region Stockholm. The study was funded by the Swedish Research Council, the Center for Innovative Medicine Foundation, and other foundations.
Some researchers report assignments for the pharmaceutical industry, which are disclosed in the scientific publication.
Anticholinergic drugs in the study were identified based on the Anticholinergic Cognitive Burden (ACB) scale, a tool used in research and clinical contexts. The scale covers a wide range of different drugs that are scored between 1 and 3, depending on how much the drug blocks the neurotransmitter acetylcholine. The consumption of these drugs is added up to estimate a patient’s anticholinergic burden. The drugs included in ACB are listed in table S1 in the study’s supplementary information.
Every day in South Africa, 30 people are shot dead. Another 43 are shot and survive. That is more than one person shot every 20 minutes, around the clock, every single day of the year.
Those numbers are staggering, but they don’t begin to convey the cascade of harm that extends beyond the bodies that take the bullets.
Consider this experience of Professor Sithombo Maqungo, head of orthopaedic trauma at Groote Schuur Hospital. A grandmother admitted with a fractured hip is scheduled for urgent surgery on Friday morning. As she is being prepped for theatre, a gunshot victim is rushed in, bleeding out. He dies, but the grandmother’s surgery is postponed as the weekend’s trauma cases overwhelm the unit. By Monday, her condition has deteriorated — blood clots, pressure sores, pneumonia. She dies. Her death certificate will not record “gunshot wound” as the cause. But she is, without question, a victim of gun violence.
This is the ripple effect of gun violence. One shooting does not claim one life. It consumes blood supplies, monopolises theatre time, depletes Intensive Care Unit beds, exhausts healthcare teams, and drives skilled professionals — paramedics, nurses, surgeons — out of a system that can no longer support them.
South Africa’s healthcare system is treating gun violence, it is not preventing it. And that distinction matters enormously.
Young men are the primary victims and perpetrators of gun violence, but women are increasingly killed with guns. After declining, following the Firearms Control Act of 2000, gun-related femicide has surged — rising 84% between 2017 and 2020/21. By 2020/21, firearms accounted for more than one-third of all femicides, the highest proportion recorded.
Failures in firearm oversight and the growth in licensed guns have contributed to this reversal.
South Africa’s own evidence shows that regulation works. When the Act was properly enforced between 2000 and 2010 — guided by a five-pillar strategy that tightened regulations and reduced the availability of firearms — gun deaths halved, from 34 people shot dead daily to 18, while a woman died at the hands of an intimate partner every eight hours rather than every six hours because fewer women were shot and killed.
As oversight weakened through under-resourcing, corruption and policy drift, deaths rose again.
Today, licence applications are 66% higher than in 2016, with a record 166,603 new applications in 2024/25 alone — expanding the pool of legally held guns that leak into criminal hands or are used to commit crimes.
Illegal guns don’t come from nowhere
A common misconception is that tightening firearm laws is pointless because most crime guns are unlicensed. But illegal guns do not appear from nowhere: virtually every firearm in criminal circulation was once legally manufactured and legally owned before it was lost, stolen, or sold into the illegal market. In South Africa, civilians are by far the biggest source of this leakage. Over the past 20 years, civilians have lost or had stolen an average of seven guns for every one lost or stolen by the police, according to South African Police Service annual reports. In 2024/25 alone, civilians reported the loss or theft of 7,895 firearms — 22 a day — and this is almost certainly an underestimate, since some owners do not report losses for fear of being charged with negligence (police reported the loss/ theft of 572 service guns in this time).
Legal guns are also used directly to commit crimes, particularly in domestic violence, where murder-suicides involving licensed firearms are well documented.
Controlling legal gun ownership is not separate from addressing gun crime — it is the primary mechanism for doing so.
The public health approach
A key question in response to South Africa’s gun violence crisis is why gun violence remains outside the core public health frameworks — and what would change if it were treated as the preventable health crisis it is.
A public health approach treats guns the way we treat other products that harm health — like alcohol and tobacco — moving the response upstream from treating wounds to preventing them by tightening controls over availability.
It would give healthcare workers, overwhelmed by the relentless flood of trauma, the ability to recognise that gunshot wounds are not inevitable but a preventable crisis dependent on political will and policy intervention.
It would create concrete opportunities for the health system to play a proactive role in prevention — screening for firearm access during domestic violence consultations to support gun removal from high-risk situations; linking young gunshot victims in surgical wards with gang exit programmes; using admission and forensic pathology data to identify violence hotspots and inform targeted policing.
It would make the true costs of gun violence visible to policymakers and the public — revealing how much is spent managing a preventable crisis on limited resources and overstretched facilities that could instead go towards primary healthcare, cancer treatment, or diabetes care. And crucially, it grounds the debate in evidence rather than ideology — vital in a post-truth world where beliefs, opinions, and hearsay are routinely presented as fact.
This approach would also recognise that firearms are a product sold for profit that harms people’s health. Just as taxes on alcohol and tobacco reflect their social costs and reduce consumption, firearms, ammunition and shooting activities should be subject to equivalent measures. This would generate revenue that could fund the very health services overwhelmed by the consequences of gun violence.
This sharpens the policy response too. South Africa’s Firearms Control Amendment Bill, currently at Nedlac, proposes strengthening limits on who can own firearms, the type and number of firearms and ammunition rounds that can be held, and for which purposes.
Treating gun violence as a public health crisis strengthens the case for these reforms: it positions the Bill not as a security measure but as a health measure, demanding the same urgent political commitment we would expect for any leading cause of preventable death and injury.
International framework
None of this can happen in isolation. South Africa needs international frameworks, evidence, and solidarity — and that is where the World Health Organisation (WHO) comes in.
On 10 February 2026, the Global Coalition for WHO Action on Gun Violence launched with more than 100 organisations across 40 countries, including a range of South African organisations spanning healthcare, child and women’s rights, legal advocacy, violence prevention, and research. The coalition’s formation was accompanied by a stark finding: not one of the World Health Assembly’s 3,200-plus adopted resolutions explicitly mentions firearms.
This is a profound gap. The WHO sets global standards that shape national health policy across 194 member states. When it fails to treat gun violence as a health priority, countries like South Africa are left without the international frameworks, evidence, and technical guidance they need to act.
The WHO has done this before, with other contested, politically sensitive issues — tobacco, HIV/AIDS, alcohol, violence against women — each time moving them from marginal concerns into mainstream public health priorities with measurable results. A resolution on road safety catalysed legislative reform in more than 100 countries. The Framework Convention on Tobacco Control contributed to lasting reductions in global tobacco use. The same is possible for gun violence.
The coalition is calling on the WHO to take ten key actions, including strengthening guidance on gun-related healthcare and supporting countries to use health systems as sites of gun violence prevention. South Africa — with some of the highest rates of gun violence in the world and a documented track record of evidence-based intervention — is uniquely placed not just to support this coalition, but to lead it by sponsoring a World Health Assembly resolution on firearm violence.
Our health professionals are close to breaking point. The surgeon who cannot cope with the relentless toll and resigns — leaving already stretched colleagues even more depleted. The paramedics who quit working in a war zone they never enlisted in. The medical students who leave the profession early, unable to bear the accumulated trauma of what they witness.
Gun violence is not inevitable. It is preventable. Treating it as a public health crisis is the only rational response to the evidence we already have.
Claire Taylor is from Gun Free South Africa, and Dean Peacock is from the Global Coalition for WHO Action. Views expressed are not necessarily those of GroundUp.
For GPs, solutions for treating osteoarthritis are frustratingly limited – it’s like the weather, everyone talks about it but nobody does anything about it. While standard care can relieve symptoms, there is currently no way to regenerate the actual lost cartilage in the joints. Some experimental treatments have proven successful in animal models and in petri dishes, but those are still many years away from being approved and available on the market.
But what if there was a currently available drug that could be repurposed? Since overweight and obesity worsen osteoarthritis symptoms by placing excess strain on weight-bearing joints, GLP-1 agonists such as semaglutide have proven that they can help by promoting rapid weight loss, as demonstrated by the STEP-9 trial.
Research into GLP-1s has now revealed that they may offer a whole constellation of other benefits, such as a potential reduction in stroke risk. Now, it appears that GLP-1 agonists may have a direct effect on osteoarthritis independent of weight loss. In our podcast, we look at a recently published article in Cell Metabolism that suggests that GLP-1 agonists might go beyond just the weight loss – promote actual cartilage regrowth by jumpstarting the joint cells’ energy processing pathways. We also explore some of the caveats of potentially using GLP-1 agonists in this way, such as a lack of understanding of the long term effects, as well as the well-documented occurrence of muscle loss.
South Africa’s public tender framework has long recognised the importance of ensuring reliable, affordable, and uninterrupted access to essential medicines and vaccines, particularly for national immunisation programmes that protect children and vulnerable populations.
While local pharmaceutical manufacturing remains an important national objective, it is equally critical that public procurement decisions prioritise patient access, programme sustainability, and fiscal responsibility, especially in vaccine supply where scale, complexity, and affordability are decisive factors.
Vaccines require scale, specialisation and reliability
Vaccine manufacturing at national immunisation scale requires highly specialised infrastructure, advanced technical capability, strict regulatory compliance, and sustained capital investment. These requirements differ materially from those of many small‑molecule medicines.
“When it comes to vaccines, the overriding priority of the public tender system must be patient access. Scale, affordability, and uninterrupted supply are essential if South Africa is to expand and sustain its national immunisation programmes,” said Simo Masondo, Chairman of the Generic and Biosimilar Medicines Association of South Africa (GBMSA).
Although South Africa has made meaningful progress in strengthening elements of local pharmaceutical capability, vaccine manufacturing readiness varies significantly across product categories, and certain capacities continue to evolve. In this context, national immunisation programme must be supported by a calibrated combination of local and global manufacturing supply, particularly where programme expansion, continuity and affordability are at stake.
A tender system that prioritises supply reliability and scale is essential to ensuring that immunisation program can reach more patients, more consistently and without interruption.
Competitive pricing and demonstrable value for money remain central to the sustainability of South Africa’s public healthcare system. The National Department of Health has consistently emphasised procurement principles that include value for money, open and effective competition, accountability, and equity.
In vaccine procurement, competitive tender outcomes directly enable:
Broader immunisation coverage
Greater reach to children and underserved populations
More efficient use of limited public healthcare resources
Affordability is not a secondary consideration; it is a core enabler of access.
BRICS partnerships as strategic enablers of vaccine access
Trusted international partnerships, particularly within the BRICS ecosystem, play a critical role in supporting South Africa’s vaccine supply objectives. Long‑standing collaborations with partners in countries such as India have consistently demonstrated scale, reliability, regulatory compliance, and significant cost efficiencies in national tenders.
Indian vaccine manufacturers have historically delivered substantial savings to the South African government, in some cases exceeding R2 billion on a single vaccine programme, while supporting the expansion and sustainability of national immunisation coverage.
These partnerships should be viewed not as alternatives to local capability, but as essential enablers of immediate access, affordability, and programme continuity, particularly in vaccine categories where local scale is still developing.
A pragmatic and patient‑centric path forward
“A pragmatic, balanced approach allows South Africa to meet today’s immunisation needs while continuing to build capability over time. This is not a choice between localisation and access; it is about sequencing decisions responsibly so that patients always come first,” Masondo said.
Such an approach ensures:
Reliable and uninterrupted vaccine supply
Expanded immunisation reach for South African children
Responsible stewardship of public healthcare funds
Long‑term programme sustainability
Strengthened international cooperation within BRICS and other trusted partnerships
By prioritising access, affordability, and scale in vaccine procurement, South Africa can protect its immunisation programmes today while continuing to build manufacturing capability over time, without compromising patient outcomes or fiscal sustainability.
Small cell lung cancer cells (green and blue) that metastasised to the brain in a laboratory mouse recruit brain cells called astrocytes (red) for their protection. Credit: Fangfei Qu
Artificial intelligence tools are increasingly being developed to predict cancer biology directly from microscope images, promising faster diagnoses and cheaper testing. But new research from the University of Warwick, published in Nature Biomedical Engineering, suggests that many of these systems may be using visual shortcuts rather than true biology – raising concerns that some AI pathology tools are currently too unreliable for real-world patient care.
“It’s a bit like judging a restaurant’s quality by the queue of people waiting to get in: it’s a useful shortcut, but it’s not a direct measure of what’s happening in the kitchen,” says Dr Fayyaz Minhas, Associate Professor and principal investigator of the Predictive Systems in Biomedicine (PRISM) Lab in the Department of Computer Science, University of Warwick, and lead author of the study.
“Many AI pathology models are doing the same thing, relying on correlations between biomarkers or on obvious tissue features, rather than isolating biomarker-specific signals. And when conditions change, these shortcuts often fall apart.”
To reach this conclusion, the researchers analysed more than 8000 patient samples across four major cancer types – breast, colorectal, lung and endometrial – and compared the performance of leading machine learning approaches. While the models often achieved high headline accuracy, the team found this frequently came from statistical “shortcuts.”
For example, instead of detecting mutations in the cancer-associated BRAF gene, a model might learn that BRAF mutations often occur alongside another clinical feature such as microsatellite instability (MSI). The system then learns to use this combination of cues to predict BRAF status rather than learning the causal BRAF signal itself – meaning accurate cancer predictions work only when these biomarkers co-occur and become unreliable when they do not.
Kim Branson, SVP Global Head of Artificial Intelligence and Machine Learning, GSK and co-author says, “We’ve found that predicting a BRAF mutation by looking at correlated features like MSI is often like predicting rain by looking at umbrellas – it works, but it doesn’t mean you understand meteorology.
“Crucially, if a model cannot demonstrate information gain above a simple pathologist-assigned grade, we haven’t advanced the field; we’ve just automated a shortcut. The roadmap for the next generation of pathology AI isn’t necessarily bigger models; it’s stricter evaluation protocols that force algorithms to stop cheating and learn the hard biology.”
When performance of AI models was assessed within stratified patient subgroups, such as only high-grade breast cancers or only MSI-positive tumours, accuracy fell substantially, revealing that the models were dependent on shortcut signals that disappear once confounding factors are controlled.
For certain prediction tasks, the performance advantage of deep learning over human-derived clinical information was modest. AI systems achieved accuracy scores of just over 80% when predicting biomarkers, compared with around 75% using tumour grade alone – a measure already assessed by pathologists.
Machine learning methods can still prove valuable for research, drug development candidate screening and for clinical triaging, screening, or supplementary decision support. However, the researchers argue that future AI tools must move beyond correlation-based learning and adopt approaches that explicitly model biological relationships and causal structure.
They also call for stronger evaluation standards, including subgroup testing and comparison against simple clinical baselines, before looking at deployment in routine care.
Dr Minhas concludes, “This research is not a condemnation of AI in pathology. It is a wake-up call. Current models may perform well in controlled settings but rely on statistical shortcuts rather than genuine biological understanding. Until more robust evaluation standards are in place, these tools should not be seen as replacements for molecular testing, and it is essential that clinicians and researchers understand their limitations and use them with appropriate caution.”
Human neutrophils visualised under a confocal microscope with cell membrane (red) and nucleus (blue). When faced with an infection during food scarcity, stress hormones trigger an immune response dependent on neutrophils, abundant cells that act as immediate, short-lived defenders. Credit: Thai Tran, National Institute of Arthritis and Musculoskeletal and Skin Diseases
When food is scarce, stress hormones direct the immune system to operate in “low power” mode to preserve immune function while conserving energy, according to researchers at Weill Cornell Medicine. This reconfiguration is crucial to combating infections amid food insecurity.
The answer could be important in helping those who are food insecure and face the risk of infectious diseases every day. “Mounting an immune response against infections requires a lot of energy. We have discovered a coordinated system that upholds immune function by shifting the composition and metabolism of immune cells,” Dr Collins said.
The results, published in Immunity, found that mice on a calorie-restricted diet fought off infection as well as mice that were fully fed, but did so while using very little glucose. This was possible thanks to glucocorticoids, stress hormones known for their role in regulating blood glucose. The researchers determined that glucocorticoids acted like master conductors, reorganizing immune cells and their energy usage to provide a survival advantage.
The research was co-led by Luisa Menezes-Silva, a visiting graduate student from the University of São Paulo, Brazil; Dr Mingeum Jeong, a postdoctoral associate; and Dr Seong-Ji Han, a research associate, all in the Collins lab at Weill Cornell.
Shifting Priorities
To understand the complex interactions involved in an immune response during scarcity, Dr Collins and his team put mice on a 50% restricted-calorie diet and then exposed the animals to bacteria that infect the gut. The mice that were fed a standard diet experienced a metabolic crash – their blood glucose levels and body weight plummeted.
The researchers had expected this would happen to all the animals because mounting an immune response can consume up to 30% of the entire body’s fuel reserves. But in the calorie-restricted mice, the immune system appeared to be functioning perfectly well without using much glucose.
To unravel this enigma, the researchers inventoried the immune cells of the infected animals and discovered that T cells, which normally target invading microbes, were depleted in the calorie-restricted mice. Instead, short-lived neutrophils, which serve as the body’s first responders to infection, were ramped up to twice the normal amount and had measurably enhanced pathogen-killing abilities. The cells seemed to be operating in energy-saving mode, consuming much less glucose than neutrophils from well-fed animals.
“So, this hormone rewires the immune system to eliminate the infection while keeping blood sugar from dropping, which rescues the calorie-restricted animals from malnutrition,” said Dr Collins.
Stress Hormones Lead the Charge
The researchers are breaking new ground by outlining how a sudden fall in food intake triggers glucocorticoid levels to rise, resulting in two major shifts. First, the body repositions certain immune cells – especially naïve T cells – into the bone marrow, which becomes a kind of “safe house” for when the cells are needed. Second, during an infection, glucocorticoids tilt the immune response away from energy‑intensive T cells toward neutrophils, abundant cells that act as immediate, short-lived defenders.
Beyond clearing a current infection, glucocorticoids prepare the immune system for repeat encounters with infectious agents. While the hormones direct killer T cells to stand down and neutrophils to step up, they also ensure memory T cells are preserved for future confrontations.
“Glucocorticoids reduce the immune cells that use up the most energy, while saving those that are critical for protection against future infections,” Dr Collins said. “So, these hormones are involved in every step of the infection-fighting process.”
“Since glucocorticoids are induced not only by nutrient restriction but also by any form of stress, our findings might have broader applicability,” said Dr Collins.
In the meantime, he and his team plan to explore what causes the system to fail when the degree and duration of calorie restriction are more severe. “We looked at reduced food intake over three weeks,” he said. “But when you cross the threshold into malnutrition, the whole system breaks down.” Understanding this collapse could inform better strategies to prevent infectious disease and infection-driven malnutrition in vulnerable populations.
Stimulating two brain areas, nudging them to collectively fire in the same way, increased a person’s ability to behave altruistically, according to a study published February 10th in the open-access journal PLOS Biology by Jie Hu from East China Normal University in China and colleagues from University of Zurich in Switzerland.
As parents raise their kids, they often work to teach them to be kind and to share, to think about other people and their needs – to be altruistic. This unselfish attitude is critical if a society is going to function. And yet, while some people grow up to devote themselves to others, other people still manage to grow up selfish.
To understand what brain areas and connections might underlie individual differences in altruism, the researchers asked 44 participants to complete 540 decisions in a Dictator Game – offering to split an amount of money with someone else, which they then got to keep. Each time, the participant could make more or less money than their partner, but the amounts varied. As the participants played the game, the researchers stimulated their brains with transcranial alternating current stimulation over the frontal and parietal lobes of the brain. The stimulation was set up to make the brain cells in those areas fire together in repetitive patterns, training them all to either gamma or alpha oscillation rhythms.
The authors found that during the alternating current stimulation designed to enhance the synchrony of gamma oscillations in the frontal and parietal lobes, the participants were slightly more likely to make an altruistic choice and offer more money to someone else – even when they stood to make less money than their partner. Using a computational model, the researchers showed that the stimulation nudged the participants’ unselfish preferences, making them consider their partner more when they weighed each monetary offer. The authors note that they did not directly record brain activity during the trials, and so future studies should combine brain stimulation with electroencephalography to show the direct effect of the stimulation on neural activity. But the results suggest that altruistic choices could have a basis in the synchronized activity of the frontal and parietal lobes of the brain.
Coauthor Christian Ruff states, “We identified a pattern of communication between brain regions that is tied to altruistic choices. This improves our basic understanding of how the brain supports social decisions, and it sets the stage for future research on cooperation – especially in situations where success depends on people working together.”
Coauthor Jie Hu notes, “What’s new here is evidence of cause and effect: when we altered communication in a specific brain network using targeted, non-invasive stimulation, people’s sharing decisions changed in a consistent way – shifting how they balanced their own interests against others’.”
Coauthor Marius Moisa concludes, “We were struck by how boosting coordination between two brain areas led to more altruistic choices. When we increased synchrony between frontal and parietal regions, participants were more likely to help others, even when it came at a personal cost.”
