Millions of people worldwide carry viral infections they acquired at birth, often for life. For a long time it was assumed that the immune system hardly fights these pathogens. Researchers from the University of Basel show now that the body’s defenses do indeed act against the virus. This could be a useful starting point for future therapies.

Modern medicine can often prevent viruses from being passed from mother to child during birth, for example in the case of the hepatitis B virus (HBV). However, once the infection is established, it still cannot be cured. More than 250 million people worldwide live with a chronic HBV infection, almost all of them since birth.

Until now, it was assumed that the immune system tolerates such infections and hardly defends itself against them. A new study by researchers at the Department of Biomedicine at the University of Basel provides evidence that the immune system fights these infections more effectively than previously thought.

“Our study changes the way we think about chronic infections that begin early in life,” says Dr. Katrin Martin, co-first author of the study published in Immunity. “We found that the immune system continues to fight the virus in adulthood with partial success, although it is, in a sense, operating with the brakes on.”

How the body responds to the virus

Using a mouse model that replicates key aspects of an infection acquired at birth, the research team examined the immune response over an extended period. The results showed that the body gradually produces antibodies that help to reduce the amount of virus. This response is supported by specialized immune cells known as T helper cells, which enable other immune cells to produce more effective antibodies.

These T helper cells are indeed active and effective in adulthood. “However, they are less frequent and less diverse than those seen in infections encountered later in life,” explains co-first author Dr. Peter Reuther. As a result, the immune response remains limited and is unable to completely eliminate the virus.

Strengthening the immune response in a targeted way

In a next step, the researchers investigated whether this limited immune response could be enhanced. In their experiments, they were able to improve the antibody response by administering additional T helper cells to the mice. This suggests that the reduced availability of T helper cells is an important limitation of the immune response to infections acquired early in life.

The researchers suspect that this is because the viral infection occurs during a sensitive phase of the immune system’s development. As a result, the formation of specific T cells remains limited, and the organism develops partial tolerance to the virus, allowing the latter to persist in the body indefinitely.

“The fact that the immune response can be enhanced by adding T helper cells is promising for the development of new therapeutic approaches,” says study leader Professor Daniel Pinschewer. “Building on existing and partly effective defense mechanisms is more promising than trying to induce an immune response that is completely lacking.”

Tiny micro- and nanoplastic fragments seem to be turning up everywhere, including one of the most well-protected parts of the human body—the brain. In a recent study conducted by Chinese researchers, they found microplastics and nanoplastics (MNPs) in nearly all the brain samples they tested, both healthy and diseased human brains.

As per the findings published in Nature Health, the microplastic levels were the highest recorded in the study, reaching 129 micrograms per gram in tumor-affected brain tissue. The healthy brain and spinal cord tissue had considerably lower levels, with a median of 50.3 micrograms per gram. While the possibility of finding microplastics in the brain cannot be denied, the actual quantities are far lower than the striking spoonful claim made during a joint announcement by the US Environmental Protection Agency (EPA) and Health and Human Services (HHS) in early April 2026.

Minuscule escape artists

Studies have found that microplastics can enter the human body through breathing, eating, and skin contact. The brain is protected by an exceptionally selective filter called the blood-brain barrier, designed to keep harmful substances out of our most vital organ. Yet previous studies have found that microplastics can somehow bypass this defense and enter the brain. This is particularly concerning because very little is known about what these foreign particles do once inside, where they go and settle, or what concentrations they can reach.

To answer these queries, the researchers used advanced tools such as high-resolution laser direct infrared spectroscopy (LDIR) and scanning electron microscopy (SEM) to examine 191 brain samples. One hundred fifty-six samples were collected from 113 living patients undergoing surgery for tumors like gliomas and meningiomas, and 35 samples from five post-mortem donors with healthy brains to see if plastic was present in normal brain tissue.

A closer look revealed that MNPs were present in almost all samples: 99.4% of diseased tissue samples and 100% of healthy tissue samples. Nanoplastics, which are smaller in size, were more abundant than microplastics. The team was even able to identify the type of plastic the tiny bits came from: PET, often used to make beverage bottles; polyethylene, commonly used in plastic bags; polyamide that makes up textiles like nylon and PVC found in plumbing and industrial equipment.

In diseased brains, levels were not uniform across the tissue, with higher concentrations near tumors, possibly due to weakened natural protection. They detected these particles in operating room environments, raising the possibility of exposure during medical procedures.

Their analysis also found that the larger the surface area of microplastics, the faster the tumor cell growth. While this doesn’t mean microplastics cause cancer, it does raise questions about the role MNPS may play in how quickly the disease progresses, an area the researchers noted requires further exploration.

Tackling MNP pollution calls for joint action from policymakers, manufacturers, and consumers. Findings from this study, along with future research, can strengthen public awareness and drive demand for change, helping to push policies grounded in evidence rather than sensationalism.

Researchers at the University of British Columbia and BC Cancer have developed a new way to target proteins long considered “undruggable,” opening the door to new treatments for prostate cancer and other serious diseases. Known as intrinsically disordered proteins, these molecular shapeshifters are extremely difficult to target with medication due to their flexible and ever-changing structure. They play a central role in a wide range of diseases—including cancer, neurodegenerative disorders, heart disease and autoimmune conditions—yet only a handful of medications currently exist that can target them.

In a study published in Signal Transduction and Targeted Therapy, the researchers demonstrate a new approach for designing drugs that bind more strongly to these proteins and block their disease-causing activity. In some cases, the compounds they developed bound up to a million times more tightly than any previously reported.

“This study shows that proteins previously thought to be undruggable can be drugged with remarkable efficacy,” said principal investigator Dr. Marianne D. Sadar, professor of pathology and laboratory medicine at the UBC faculty of medicine and distinguished scientist at BC Cancer.

“The findings could have profound implications for the treatment of cancer and other diseases, providing a roadmap for the development of new treatments.”

A long-standing challenge in drug discovery

Unlike most proteins, which fold into stable three-dimensional shapes, disordered proteins contain flexible regions that change as they interact with molecules inside cells. Because they lack fixed binding sites, they are extremely difficult to target with traditional drugs.

“Most drug discovery is like designing a key for a very specific lock,” said Dr. Sadar. “But disordered proteins don’t behave like locks at all, they’re more like moving strands of spaghetti.”

Dr. Sadar and her team have spent decades studying how to target these proteins. In 2008, they developed the first compound capable of binding to them, and have since advanced two such drugs into clinical trials—another world-first milestone for the field.

Despite these advances, achieving strong and consistent binding has remained a central challenge.

A new strategy against prostate cancer

The new study focused on a specific protein, the androgen receptor, which fuels the growth of most prostate cancers.

Rather than fitting into a single fixed spot, the researchers developed compounds that interact with the moving region of the protein, freeze it in an inactive state, and prevent it from turning on genes that drive cancer growth.

“It’s a major achievement. Our target drugs had binding affinity a million times greater than existing drugs targeting these regions,” said Dr. Natalie Strynadka, professor of biochemistry and molecular biology at the UBC faculty of medicine.

By systematically modifying the compounds at the molecular level, the researchers identified several promising candidates that effectively shut down the receptor. In animal studies, several compounds slowed prostate cancer growth more effectively than a commonly used prostate cancer treatment.

“What surprised us was how effectively these molecules could attach to a protein that doesn’t have a fixed structure,” said Dr. Raymond Andersen, professor in UBC’s department of chemistry. “We were able to shut down the androgen receptor even in situations where current prostate cancer drugs stop working.”

The researchers now aim to advance the most promising candidates toward clinical trials, with the goal of developing prostate cancer drugs that can be used earlier in treatment and with fewer side effects. Because disordered proteins are involved in many diseases, they say the approach could have a much broader impact.

“If the approach continues to prove successful, it could dramatically expand the number of proteins that scientists can target with medicines—turning what was once considered a dead end into a promising new frontier for drug discovery,” said Dr. Sadar.

Scientists have found that teenagers and adults living with bipolar disorder face a higher risk of early death compared to people of the same age and sex who do not have the condition. In a recent large population-based study published in JAMA Network Open, scientists looked back at existing records from Taiwan’s national health and death registries and found that people with bipolar II disorder had a 1.6 times higher risk of death from both natural causes, such as medical illnesses, and unnatural causes, such as accidents and suicide.

How big are the risks?

Bipolar disorder (BP) is a mental health condition where a person’s mood, energy, and ability to cope with daily life can shift dramatically over time. These changes come in episodes that can last for several days or even weeks, where one’s mood becomes unusually high, overly energetic, or sometimes very irritable.

At the other end of the spectrum, during depressive episodes, people with BD feel intense sadness to a point where their ability to experience disappears. This isn’t a rare condition, as one in 200 people around the world live with some form of BD.

A team of Taiwanese researchers analyzed data from over 11,000 people with bipolar II disorder (BD-II) to understand their long-term risk of early death. This condition involves both depressive episodes and hypomanic episodes of elevated mood and energy. These symptoms are usually less severe than in bipolar I disorder (BD-I), where manic episodes can sometimes become so intense that hospital care is required.

The study included participants aged 12 and older who had been professionally diagnosed with BD-II, and about 62% were women. For comparison, it also included 45,708 people without the disorder. The study collected data from between 2001 to 2022, and where the average follow-up time across all participants was around 7.3 years.

Statistical modeling revealed that people with BD-II were about 60% more likely to die from any cause compared to people of the same age and sex without the condition. The risk of death from physical illnesses—such as heart, lung, and digestive diseases—was also 37% higher than in the general population.

In addition, they were nearly 4.5 times more likely to die from unnatural causes, including accidents, suicide, or violence. They also found that people with BD-II actually had a 24% higher risk of death overall compared to those with BD-I but the risk from unnatural causes was not very different.

The special focus on BD-II was needed because, for a long time, it wasn’t clear whether it carries a separate risk of early death. Many earlier studies grouped BD-II together with BD-I, making it difficult to understand the risks specific to BD-II and leaving doctors without the clarity they need to identify warning signs earlier and improve treatment plans.

The researchers note that the study makes a compelling case that BD-II carries a significant risk of early death across a wide range of causes, highlighting just how urgently people with this condition need comprehensive and proactive psychiatric care.

While these findings are important, they do come with limitations worth noting. The data came exclusively from a Taiwanese population, which limits how broadly the results can be applied elsewhere, and lacked information on mood severity, episode frequency, and lifestyle habits, all of which can influence mortality risk.

Further research addressing these gaps is needed to guide evidence-based, integrated psychiatric and medical care for people with BD-II.

For decades, neuroscientists have been trying to uncover the neural processes that allow humans and various other animals to recall emotional experiences of past events. Past studies have identified a network of brain regions that support the encoding and consolidation of these memories. These regions include the hippocampus and the amygdala, as well as the para-hippocampal, perirhinal, prefrontal, parietal and retrosplenial cortices.

Researchers at Neuroscience NeuroSU and the Institute of Biology Paris-Seine- IBPS carried out a study on rats aimed at better understanding how the dorsal and ventral hippocampus, two segments of the hippocampus known to have different functions, contribute to the consolidation of emotional memories of past events.

Their findings, published in Nature Neuroscience, suggest that these two regions coordinate during sleep to consolidate memories of past experiences and the emotions associated with them.

“We already knew a lot about the role of sleep-dependent reactivation in the dorsal hippocampus, but comparatively much less is known about the ventral part of the hippocampus,” Gabrielle Girardeau, senior author of the paper, told Medical Xpress.

“In addition, it was previously shown that the dorsal part of the hippocampus communicates during sleep with other structures related to emotions, like the amygdala. However, the anatomy shows that the dorsal hippocampus is not connected to these structures.”

How rats process emotional experiences while sleeping

Earlier neuroscience studies found that the dorsal hippocampus is not connected to other brain regions associated with the processing of emotions. This suggests that it communicates with these regions via an intermediate brain region when consolidating emotional memories of past events.

Girardeau and her colleagues hypothesized that this intermediate region is the ventral hippocampus, the other segment of the hippocampus. Contrarily to the dorsal hippocampus, this region is known to communicate with emotion-processing brain regions.

“We hypothesized that the dorsal and ventral parts of the hippocampus coordinate during sleep to associate contextual and emotional information, and potentially mediate the communication with the rest of the emotional network,” said Girardeau. “We wanted to test this, as it was not known how dorso-ventral communication occurred during sleep following emotional experiences.”

To test their hypothesis, the researchers carried out a series of experiments involving freely moving rats. These rats had tiny electrodes implanted in their brains, which recorded the activity of many neurons simultaneously both in the dorsal and ventral hippocampus.

“We collected electrophysiological recordings while the rats were undergoing an emotional experience, and then sleeping,” explained Girardeau. “We used computational methods to analyze the activity of these neurons and examine how they coordinate/dialogue during sleep, and how accurately this coordination reflects the preceding emotional experience.”

While they were awake, some rats experienced a small electric shock, while others received a reward. The researchers looked at the activity of neurons in the dorsal and ventral hippocampus both during these experiences and after them, while the rats were sleeping.

“We observed neural reactivation (a phenomenon known to support sleep-dependent memory-processing) during sleep that spans the entire axis of the hippocampus following an emotional positive or negative experience,” said Girardeau.

Towards a better understanding of emotional memory consolidation

The recordings collected by this research team confirmed that while rats are sleeping, their brain consolidates memories of emotional experiences they had while awake. The consolidation of both aversive and pleasurable experiences appears to be supported by coordinated activity between the dorsal and ventral hippocampus.

“We also found that reactivation is more faithful to the original experience when the experience was negative,” said Girardeau. “This might explain the bias towards better memories of negative compared to positive events. More broadly, it identifies a mechanism that allows us to form memories combining context and emotions, positive or negative.”

If validated in humans, the results of this recent study could help to shed more light on the intricate neural processes that support the consolidation of traumatic memories and could play a role in trauma-related mental health conditions. For instance, they might improve the understanding of post-traumatic stress disorder (PTSD) and other mental health disorders that are linked to intrusive and sometimes debilitating memories of traumatic events.

“We are now planning to move beyond the hippocampus and extend our understanding of cross-area communication involved in emotional-memory consolidation to other structures like the amygdala or prefrontal cortex,” added Girardeau. “We also hope to understand how stress might additionally influence these sleep-dependent processes.”

How can ADHD be both a source of daily struggle for millions and a common trait among highly accomplished artists and innovators like Justin Timberlake and Simone Biles? The science behind this paradox is the focus of new research from Constructor University neuroscientist Dr. Radwa Khalil published in iScience, which explores the shared neurological mechanisms that connect creativity and attention. The study demonstrates how certain cognitive processes associated with ADHD—such as defocused attention—can also be potent sources of creative thinking when properly harnessed.

The study, co-authored by researchers from several prestigious French research institutions, offers promising prospects for creative therapies that use things like art, music and dance as effective, non-pharmacological interventions for the nearly 8% of children worldwide affected by ADHD.

According to Dr. Khalil, the findings signal a shift in thinking about ADHD. “There’s a tendency to view attention-related conditions like ADHD purely through the lens of deficit: what is wrong, what is missing, or what needs to be fixed?” she said. She explained that while ADHD is often viewed as a deficit, new insights reveal that attention and creativity share neural networks. “Neurodivergent attention patterns, then, are not merely problems. They can open pathways to powerful creative thinking when directed appropriately.”

The article, titled “Attention Unleashed: creative therapy for thoughtful transformation,” synthesizes research from several disciplines to illustrate how creativity and attention processing involve overlapping neural networks. It further explains how free-associative thinking patterns that spark creative ideas are also associated with distractibility, mind-wandering and other behaviors commonly observed in ADHD.

Dr. Khalil offered an analogy to help clarify the connection: “Think of attention like a spotlight. Most people are able to focus their beam on one thing. ADHD brains have a wider spotlight, taking in more information at once. This condition can make routine tasks that require focus challenging. However, this broader view, or ‘defocused attention,” also encourages exploratory thinking and new idea combinations, which fuel creativity.”

Dr. Khalil and her colleagues see promising and practical therapeutic implications for those with ADHD and related disorders. Methods involving creative activities like art, music, dance, writing, gaming and more can provide structured opportunities for individuals with ADHD to channel and explore their defocused attention. Creative activity may also help strengthen the neural networks involved in attention control, rewiring patterns that contribute to traits like impulsivity and hyperactivity.

“Authentic creative expression is so much more than a pleasant distraction,” continued Dr. Khalil. “It is engaging the same neural circuits involved in attention control, essentially providing a workout for the brain. For a child with ADHD, the experience of getting ‘lost in the moment’ when creating art or playing music may actually be strengthening their ability to focus by working with their natural cognitive style instead of against it.”

While the outlook is promising, Dr. Khalil and her colleagues note that the link between attention and creativity remains only partially understood. To address this challenge, the article proposes a framework with detailed recommendations for advancing research, focusing on interdisciplinary collaboration, methodological innovation and longitudinal studies. Dr. Khalil emphasizes that fundamentally shifting ADHD treatment requires first establishing a comprehensive, interdisciplinary research agenda that unites neuroscientists, art therapists, clinicians and other professionals.

Depression is a debilitating mental health disorder that is estimated to affect approximately 5% of people worldwide. It is characterized by persistent feelings of sadness and hopelessness, a lack of interest in everyday activities, sleep disturbances, and possible changes in appetite. There are now several treatments for depression, including medications such as selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs), as well as cognitive behavioral therapy (CBT) and other psychotherapeutic approaches. While many people diagnosed with depression respond well to one or more of these treatments, some experience few or no benefits.

Over the past decades, researchers have thus been trying to identify alternative treatments that could benefit patients who are resistant to available medications. Some recent studies suggest that psychedelic drugs—particularly a compound known as psilocybin, found in some mushrooms—could be effective in easing symptoms of depression.

Researchers from the University of Pennsylvania, Vrije University Amsterdam and other institutes recently reviewed 15 clinical trials assessing the potential of psilocybin as a treatment for depression. Their paper, published in Nature Mental Health, statistically combines the results of these trials, while also summarizing the experimental methods they relied on and their limitations.

“Depression is a growing and widespread debilitating illness, yet novel treatments are lacking,” Parker Singleton, first author of the paper, told Medical Xpress. “We sought to understand the current evidence base of psilocybin therapy for depression, while committing to updating our review periodically so that it remains up to date with the rapidly progressing field.”

Combining the results of 15 past studies

Singleton and his colleagues analyzed a total of 15 past randomized controlled trials, clinical trials in which people diagnosed with depression were randomly assigned to either an experimental or control group. People in the experimental group were treated with psilocybin, while those in the control group were given a different antidepressant, a placebo drug (e.g., a sugar pill), or a very low dose of psilocybin.

The researchers found the papers for their review on an open-access research database. The 15 studies they examined collectively included data collected from 801 participants. In their meta-analysis, the researchers examined the findings of only 12 of the studies, with a total of 585 participants.

“We searched through thousands of search results from scholarly databases to identify 15 randomized controlled trials of psilocybin for depression,” explained Singleton. “We extracted all depression-related outcomes from these trials and include them in our new publicly released database. We used meta-analytic modeling to synthesize the evidence across these trials and to identify aspects of trial design that contribute to heterogeneity in the literature.”

Across the studies examined by the researchers, psilocybin was found to significantly reduce symptoms of depression compared to the other antidepressant or inactive compounds they were compared to. Despite their promising results, the team observed that the studies had small sample sizes and highlighted the need for larger, more rigorous clinical trials.

Towards new promising treatments for psychiatric disorders

The recent work by Singleton and his colleagues could soon inspire further research assessing the potential of psilocybin as an antidepressant. The study limitations identified by the researchers and the recommendations included in their paper could help to plan more reliable large-scale clinical trials.

“Psilocybin for depression research is progressing rapidly,” said Singleton. “Four trials were published in 2025 alone, with several more anticipated this year. While traditional reviews quickly become outdated, our living review will be updated annually, ensuring that new evidence is reflected in the findings.”

The team are actively involved in a project called SYPRES (Synthesis of Psychedelic Research Studies). As part of this project, they published an interactive online dashboard and database that summarizes the latest findings in this field, also including programming code, clinical data, and other information that can be used by researchers who are conducting psychedelics-related mental health research.

“As part of the SYPRES initiative, we will now be covering more areas of the clinical psychedelic literature,” added Singleton. “We’ve already released another pre-printed review paper focusing on MDMA for PTSD treatment.”

Obsessive compulsive disorder (OCD) is a mental health condition characterized by recurring intrusive thoughts (i.e., obsessions) and repetitive behaviors (i.e., compulsions) aimed at reducing anxiety. This disorder is estimated to affect 1.2% to 2.3% of people every year.

While several past studies have investigated the neural, genetic and environmental factors that contribute to the emergence of OCD, these have not yet been clearly elucidated. Traumatic events, such as assaults, car accidents and other distressing experiences, have been found to play a role in post-traumatic stress disorders (PTSD) and some other mental health disorders, yet their relationship to OCD remains poorly understood.

Researchers at Karolinska Institute and Stockholm Health Care Services recently analyzed a large pool of mental health-related data collected in Sweden to explore the link between different traumatic events and the risk of developing OCD. Their paper, published in Nature Mental Health, reports an association between assaults or victimizations and a higher risk of OCD.

Exploring the relationship between trauma and OCD risk

The authors of this recent paper analyzed data collected in Sweden in the period spanning from 1975 to 2008 as part of a large cohort study. This data included official reports of traumatic events, such as assaults and transport accidents, as well as mental health records.

The researchers analyzed data related to 3.3 million individuals living in Sweden. They specifically looked at whether people who reported being assaulted or victimized and those who were involved in a transport accident were later diagnosed with OCD, comparing the mental health reports of people who experienced trauma with those of people who did not.

“The causal link between potentially traumatic events and OCD remains unclear due to reliance on retrospective self-reports and limited control for familial factors,” wrote Josep Pol-Fuster and his colleagues in their paper. “In this Swedish population-based cohort study, we identified 3,340,945 individuals born between 1975 and 2008 and prospectively examined the associations of objectively recorded assault/victimization and transport accidents with subsequent OCD diagnoses.”

The team’s analyses also included sibling comparisons, as this allowed them to control for effects linked with genetics, upbringing and other family-related factors. Ultimately, they used an approach called genetic modeling to estimate how much the risk of developing OCD arose from genetics and how much was linked to environmental factors.

“Individuals exposed to assault/victimization, but not transport accidents, had an increased OCD risk, especially within the first year, decreasing thereafter,” wrote Pol-Fuster and his colleagues. “The association persisted in discordant full sibling comparisons. Quantitative genetic modeling indicated that the phenotypic correlation was primarily due to additive genetics (69%) and unique environmental factors (31%).”

The implications for mental health research

Overall, the findings of this study suggest that assault and victimization are linked with a significantly greater risk of OCD, particularly within the year following a traumatic event. In addition, the team’s estimates suggest that most of the association between trauma and OCD is explained by genetic factors, while environmental experiences play a smaller—although still substantial—role.

“These findings highlight a complex relationship between assault/victimization and OCD, involving both genetic vulnerability and individual environmental exposure,” wrote the authors.

This research could inspire more studies focusing specifically on the relationship between being assaulted or victimized and the emergence of OCD. Concurrently, it could help to improve psychological services: for instance, informing the development of services designed to support victims of assaults or other violent crimes immediately after a traumatic event.

Researchers at the School of Medicine at the University of California, Riverside have discovered previously unrecognized immune surveillance structures in the skin. Found within hair follicles, the cells resemble M (microfold) cells—specialized epithelial cells traditionally associated with the gut and airway tissues.

The findings, published in Frontiers in Cell and Developmental Biology, suggest that the skin may use specialized “sentinel” cells located within hair follicle structures to monitor environmental exposure and microbial presence, expanding current understanding of how barrier tissues defend the body. The work was done in mice.

Senior author Dr. David Lo, a distinguished professor of biomedical sciences, explained that unlike the gut and airway epithelium, which consists of a single-cell layer allowing relatively direct environmental sampling, the skin is composed of multiple stratified layers that form a more robust physical barrier.

“This raises a long-standing question in immunology: how does the skin efficiently monitor external threats despite its thickness?” Lo said.

Lo’s team proposes that hair follicles may act as localized “gateway” structures that concentrate both environmental material and immune sensing activity. Within these niches, the team identified M cell-like sentinel cells that appear to participate in localized immune responses, particularly to Gram-positive bacteria—bacteria that can cause a range of infections, from food poisoning to serious respiratory diseases.

“Hair follicles may represent a central hub for immune surveillance in the skin,” said Diana Del Castillo, the first author of the paper and a graduate student in Lo’s lab. “These structures bring together environmental exposure, immune sensing, and potentially even neural signaling in a highly localized environment.”

While the research team is still characterizing the cells, early findings suggest they are part of a broader category of epithelial surveillance mechanisms that may exist across multiple tissues.

The discovery also raises new questions about how immune and sensory systems may be integrated. Hair follicles are already known to contribute to touch sensation, and the newly identified structures appear to be in regions closely associated with nerve endings, suggesting a potential link between immune detection and sensory signaling.

Lo said future work will focus on detailed anatomical mapping of these cells, particularly in whisker follicles in animal models since whiskers have dense innervation and complex structure.

“We would like to better understand how these cells interact with surrounding nerve and immune cells, and whether similar systems exist in humans,” he said.

Although the study is still in early stages, the findings may have future implications for understanding skin infections, immune disorders, and the development of topical therapeutics.

“We’re only beginning to understand how these systems are organized,” Lo said. “But they suggest the skin is far more dynamically involved in immune surveillance than previously thought.”

Del Castillo said the study highlights a potential shift in how scientists view barrier tissues—not as passive protective layers, but as active and highly specialized sensory and immune interfaces.

“Our study adds to growing evidence that epithelial barriers across tissues share more diverse and dynamic immune-related functions than previously recognized, particularly in their ability to respond rapidly to microbial stimuli,” she said.

Lo and Del Castillo were joined in the study by Hannah Kim and Sumaya Troy Alaama.

The research was supported by funds from the UCR School of Medicine.

The title of the paper is “Evidence for murine cutaneous immune surveillance localized to hair follicle epithelium.”

The World Health Organization announced Friday that it had given prequalification approval to a malaria treatment for newborns and infants for the first time.

Artemether-lumefantrine is the first antimalarial formulation designed specifically for the youngest victims of the mosquito-borne disease.

“The prequalification designation indicates that the medicine meets international standards of quality, safety and efficacy,” the WHO said in a statement.

Up to now, infants have been treated with formulations intended for older children—carrying a greater risk of dosage errors, side effects and toxicity.

“For centuries, malaria has stolen children from their parents, and health, wealth and hope from communities,” said WHO chief Tedros Adhanom Ghebreyesus.

“But today, the story is changing. New vaccines, diagnostic tests, next-generation mosquito nets and effective medicines, including those adapted for the youngest, are helping to turn the tide.

“Ending malaria in our lifetime is no longer a dream—it is a real possibility, but only with sustained political and financial commitment. Now we can. Now we must.”

In 2024, there were an estimated 282 million malaria cases and 610,000 deaths in 80 countries, according to the WHO.

Africa accounts for 95% of cases and deaths, with children under five accounting for three-quarters of those deaths.

The UN health agency says progress against malaria is being hampered by drug resistance, insecticide resistance, diagnostic failure and sharp reductions in foreign aid spending.

The WHO said its prequalification would enable public sector procurement and help close a long-standing treatment gap for around 30 million babies born each year in malaria-endemic areas of Africa.

Globally, 70% of countries do not have regulatory systems that are robust enough to oversee medicines, vaccines, tests and medical devices.

The WHO prequalification program ensures that key health products for international procurement meet global standards of quality, safety, efficacy and performance.