A shortage of one common nutrient could help cancer cells and viruses hide from the immune system. Researchers at Rockefeller University found that a shortage of arginine, an amino acid obtained from food and produced by the body, can interrupt the cellular machinery needed to make MHC-I proteins. These proteins act as a surveillance system, [...]A protein called TRAILshort may act as a central immune brake that limits T-cell responses and CAR-T therapy. Cancer cells can weaken the immune system by producing a protein that prevents its most important defenders from attacking. Mayo Clinic researchers have identified how this protein works, revealing a possible target for treatments designed to improve [...]T cells may use a previously unknown CD64-dependent pathway to attack acute myeloid leukemia. T cells are generally thought to identify cancer through a well-established molecular recognition system. Yet when researchers removed a key part of that system from acute myeloid leukemia (AML) cells, the immune cells continued killing them. The unexpected result led scientists [...]Over the past couple of weeks, my immune system has been struggling to fight off a cold. It’s been unpleasant, as all colds are. But throughout this time—in defiance of my plight—I’ve been waging my own war against immune systems, thanks to Pathogenic, a new roguelite twin-stick shooter from developer Aberrant Labs.
As I've downed endless shots of ineffective cough syrup, I’ve done little else with my free time than repeatedly take on the role of a bodily invader. And let me tell you: Being on the enemy’s side is much more fun. Really fun, as it turns out.
Action roguelites are a dime a dozen these days, and it takes something special to stand out. So as quiet Internet whispers turned into widespread cacophonous praise—the little indie game quickly racked up 100,000 sales and an “overwhelmingly positive” review score on Steam—I set aside my default skepticism and gave it a shot.
© Aberrant Labs/Slug Disco
A natural supplement strengthened lasting anticancer immune responses in obese mice. Weight loss can improve many aspects of health, but the immune system may not recover as quickly. Obesity can leave behind long-lasting changes in the bone marrow, where immune cells are formed, potentially weakening the body’s ability to respond to cancer even after excess [...]Researchers have found that the natural compound spermidine can help improve vaccine responses in older adults by reducing molecular markers of immune system aging. A vaccine shot can look the same from one arm to the next, but the immune system beneath the skin may not respond with the same force. In older adults, that [...]New research suggests aging ovaries may help shape inflammation across the body.The causes of inflammatory bowel disease (IBD) are poorly understood, but now, scientists have pinpointed a runaway immune response that may underlie the condition in some patients.
IBD, which is characterized by chronic inflammation in all or part of the digestive tract, affects millions of people worldwide. Its principal forms are Crohn's disease, which can occur at any point of the gastrointestinal tract, and ulcerative colitis, which affects only the colon and rectum.
While IBD patients may experience similar inflammation, the underlying cause may be different. Understanding those differences could potentially unlock new, targeted angles for treatment, researchers concluded in the new study.
"Identifying these patients early could eventually allow clinicians to move more quickly toward therapies that address the specific mechanism of disease rather than relying on a trial-and-error sequence of medications," Dr. Brad Pasternak, medical director of the IBD Clinic at Phoenix Children's Hospital, who was not involved in the work, told Live Science in an email.
The genetics of IBD are complex, with past studies linking the condition to 300 "hotspots" throughout the genome. The strongest known genetic risk factor for ulcerative colitis is a gene variant called HLA-DRB1*01:03, but how this variant contributes to IBD has been unclear.
The new study, published June 10 in The New England Journal of Medicine, helps connect the dots.
A major clue had emerged in previous research by the same team, which tested the blood of two children with IBD. The kids had autoantibodies — immune proteins that target the body itself rather than germs — that were neutralizing a key anti-inflammatory protein called interleukin-10 (IL-10).
IL-10 normally works by inhibiting the secretion of pro-inflammatory proteins, so patients whose bodies block IL-10 are effectively releasing a brake that should be holding off inflammation, Pasternak said.
The researchers suspected that these autoantibodies could be one factor causing IBD. In their latest study, they sought to find out whether more IBD patients had the same autoantibodies.
The study included data from over 4,900 people with IBD and over 1,000 without the condition. Using two separate lab tests, the researchers analyzed blood samples from both groups, finding the autoantibody in 173 of the IBD patients, or about 3.5%. The autoantibody was virtually absent from the blood of the comparison group.
Then, in lab experiments, the team exposed immune cells to blood from the IBD patients who carried the autoantibody. This lowered the amount of IL-10 while triggering a pro-inflammatory response.
Study co-author Dr. Holm Uhlig, a pediatric gastroenterologist at the University of Oxford, told Live Science that identifying what drives the formation of the autoantibodies will be "a question of intense interest." For now, though, their data suggests that patients carrying HLA-DRB1*01:03 are far more likely to have autoantibodies blocking IL-10 than those without the variant.
Historically, the variant has been associated with severe IBD that can require major surgery to treat. "Currently, autoimmune responses are not at all part of the therapeutic repertoire, and that's why we feel it's a relevant study," Uhlig said.
Uhlig also noted that the subgroup of 3.5% of patients they identified is a "significant number," given the large overall number of IBD patients worldwide.
In general, many IBD patients are currently treated with therapies that broadly suppress inflammatory pathways, Pasternak said, but not everyone responds to treatment. This study points to a potential way to someday tailor treatments to the mechanism driving specific patients' diseases, he said.
Aside from offering personalized treatments for IBD patients, Uhlig said their findings may improve diagnoses.
"Patients could undergo genetic testing already in the early stage of their disease diagnosis," he said, "and then it would determine their susceptibility to develop autoantibodies."
This article is for informational purposes only and is not meant to offer medical advice.
A new study overturns long-held assumptions about the cause of the rare inflammatory disorder MKD, identifying a previously overlooked immune defect. Why does a routine infection trigger dangerous inflammation in some people? Researchers studying mevalonate kinase deficiency (MKD), a rare inherited autoinflammatory disorder, may have finally found the answer. Scientists at the Garvan Institute of [...]In an era marked by remarkable advances in antiretroviral therapy (ART), the survival and quality of life of individuals living with HIV have dramatically improved. Yet, new research is now illuminating the complex interplay between immune system dysregulation and the emergence of cardiovascular disease (CVD) in a particularly vulnerable population: adolescents infected with HIV perinatally. A groundbreaking study, published in Nature Communications, spearheaded by Alles, Gunasena, Kettelhut, and colleagues, sheds light on the critical role of natural killer (NK) cell dysfunction in potentiating cardiovascular complications among these young patients, even while on effective ART.
Perinatally acquired HIV represents a unique clinical challenge, as infection occurs during a critical window of immune system development. While ART suppresses viral replication effectively, it does not fully restore immune homeostasis. This dysregulation manifests not only in the persistence of immune activation but also in aberrant immune cell profiles, including those of natural killer cells—a subset of lymphocytes crucial in antiviral defense and immune surveillance. The new findings suggest that disturbances in NK cell function are more than mere epiphenomena; they could actively contribute to the pathogenesis of cardiovascular abnormalities in this patient group.
The study emphasizes that NK cells in adolescents with perinatal HIV exhibit marked phenotypic and functional changes compared to age-matched uninfected controls. These alterations include impaired cytotoxic activity and aberrant expression of activating and inhibitory receptors. Such changes compromise the ability of NK cells to regulate inflammation and eliminate infected or damaged cells, fostering an environment conducive to vascular injury and endothelial dysfunction. This mechanistic insight is critical, as endothelial health is a cornerstone of cardiovascular stability.
By integrating immunophenotyping, functional assays, and clinical cardiovascular assessments, the researchers drew a comprehensive picture linking NK cell abnormalities with early signs of CVD. The adolescents studied demonstrated increased arterial stiffness, altered lipid profiles, and biomarkers indicative of systemic inflammation—all hallmarks of an accelerated atherosclerotic process. Intriguingly, these cardiovascular perturbations persisted despite sustained viral suppression, highlighting that viral load alone cannot explain the heightened cardiovascular risk.
The pathophysiology proposed by the authors centers on a chronic, low-grade inflammatory milieu driven, in part, by dysfunctional NK cell signaling. Typically, NK cells modulate inflammation through cytokine secretion and direct cytolysis of aberrant cells, maintaining tissue homeostasis. However, dysregulated NK cells may either fail to contain inflammatory stimuli or contribute to pathological immune activation. This shift not only exacerbates endothelial dysfunction but may induce vascular remodeling and fibrosis, setting the stage for premature cardiovascular disease.
Molecular analyses revealed upregulation of several pro-inflammatory pathways within NK cells isolated from affected adolescents. Notably, transcriptional profiles highlighted increased expression of genes involved in inflammasome activation, oxidative stress responses, and cell senescence markers—factors strongly implicated in vascular pathology. These insights open avenues for targeted therapeutic interventions aimed at restoring NK cell function and interrupting the inflammatory cascade implicated in CVD progression.
Importantly, the study’s implications go beyond HIV care alone. The concept that immune cell dysfunction can independently drive cardiovascular disease adds a crucial dimension to our understanding of immune-mediated comorbidities. It underscores the necessity of holistic medical care approaches that address the immunological underpinnings of chronic disease states, especially in populations with lifelong exposure to immunological stressors like perinatal HIV.
The findings also raise compelling questions about the adequacy of current ART regimens in mitigating long-term non-AIDS complications. While ART excels at viral suppression, it may not sufficiently address immune reconstitution or the correction of immune cell dysregulation. Future therapeutic strategies might need to incorporate immunomodulatory agents that specifically target NK cell pathways or inflammatory mediators to reduce cardiovascular risk.
Moreover, this study highlights the pressing need for comprehensive cardiovascular screening in adolescents with perinatally acquired HIV. Traditional risk assessment paradigms may not capture the unique pathophysiological mechanisms at play in this population. Early detection of subclinical vascular changes could catalyze timely preventative interventions, potentially improving long-term outcomes.
From a broader perspective, the research invites a re-examination of how chronic infections shape the immune landscape over an individual’s lifespan and influence multisystem disease trajectories. It suggests a paradigm where the immune system’s ongoing attempts to control persistent infection or immunologic insults inadvertently promote collateral tissue damage, exemplified here by cardiovascular impairment.
Technological advances in multi-omics and single-cell profiling have been pivotal in unraveling the nuanced dysfunctions within NK cell subsets elucidated by this work. These tools enable high-resolution mapping of immune cell states and their interactions with the vascular microenvironment, fostering a deeper mechanistic understanding that might have remained elusive with conventional methods.
The involvement of NK cells in this context may also intersect with other immune-mediated pathways, including those involving T cells and monocytes/macrophages, which together orchestrate the inflammatory response underpinning atherosclerosis. Understanding these intricate cellular crosstalk networks will be crucial to designing effective immunotherapies.
In light of this evidence, interdisciplinary collaboration between immunologists, cardiologists, and infectious disease specialists becomes more imperative. Integrating expertise from these domains can accelerate the translation of these findings into clinical interventions that mitigate cardiovascular risk among HIV-infected youth, and perhaps beyond.
Finally, this research presents an urgent call to the global health community to prioritize long-term monitoring and holistic management strategies for adolescents living with perinatal HIV. As their life expectancy approaches normality, addressing comorbid conditions such as cardiovascular disease will be essential to ensuring not just survival but sustained health and quality of life.
In summary, the pioneering study by Alles and colleagues illuminates a previously underappreciated contributor to cardiovascular disease risk in adolescents with perinatally acquired HIV on antiretroviral therapy. The demonstration that NK cell dysregulation may be a key mechanistic driver of early vascular pathology underscores the necessity for innovative therapeutic approaches targeting immune dysfunction beyond viral suppression alone. This work marks a significant advance in understanding the complex interdependencies between chronic viral infection, immune regulation, and cardiovascular health, and sets the stage for transformative changes in clinical practice and research paradigms.
Subject of Research:
Natural Killer (NK) cell dysfunction and its role in cardiovascular disease development in adolescents with perinatally acquired HIV undergoing antiretroviral therapy.
Article Title:
NK cell dysregulation may potentiate cardiovascular disease in adolescents with perinatally acquired HIV on antiretroviral therapy.
Article References:
Alles, M., Gunasena, M., Kettelhut, A. et al. NK cell dysregulation may potentiate cardiovascular disease in adolescents with perinatally acquired HIV on antiretroviral therapy. Nat Commun (2026). https://doi.org/10.1038/s41467-026-74602-y
Image Credits: AI Generated
Scientists identified an autoimmune mechanism linked to a major IBD risk gene, opening the door to targeted diagnosis and personalized therapies for thousands of patients. For decades, inflammatory bowel disease (IBD) has been treated as a single disorder, even though patients often experience dramatically different symptoms, disease courses, and responses to therapy. A new study [...]
A rare inflammatory condition linked to tattoos is appearing more often in Australia.Scientists have identified supermagnetic macrophages in the livers of homing pigeons (Columba livia domestica) that appear essential for navigation when the Sun is not visible, pointing to an entirely new mechanism for animal magnetoreception.
The post Pigeons May Sense Earth’s Magnetic Field Using Superparamagnetic Immune Cells in Their Livers appeared first on Sci.News: Breaking Science News.
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