How Immune System Attacks Contribute to Prolonged Coronavirus Infections

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Exploring autoimmune responses during coronavirus infections

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Emerging research indicates that prolonged COVID-19 infections may stem from the immune system attacking healthy tissue. Insights from four recent studies highlight autoimmunity as a potential contributor, especially in cases where intense pain is a prominent symptom.

This revelation could pave the way for urgently needed treatments, currently non-existent in the UK and US. “We must explore removing antibodies from patients to see if symptoms abate,” asserts Niels Eikelkamp from Utrecht University, Netherlands.

<p>While most individuals infected with SARS-CoV-2 recover swiftly, a subset experiences prolonged symptoms lasting months or years. Common complaints include fatigue, chronic pain, brain fog, and excessive tiredness following minimal exertion.</p>
<p>Researchers have pinpointed various potential mechanisms behind long COVID, such as persistent SARS-CoV-2 presence and gut microbiome dysfunction. These factors may be involved in diverse combinations within individuals, complicating the search for effective universal treatments.</p>
<p>A frequently discussed mechanism is autoimmunity, in which the immune system mistakenly targets the body. Typically, antibodies are designed to eliminate pathogens; however, autoantibodies can erroneously attach to the body’s own cells.</p>
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<p>Initial indications of autoantibodies playing a role in prolonged COVID-19 cases emerged from studies conducted in 2023. Apheresis treatments on individuals with long-term coronavirus infection showed reductions in autoantibody levels and improvements in symptoms, yet the exact substances responsible remain undetermined due to the broad spectrum of removals.</p>
<p>Eikelkamp and his team now provide robust evidence that autoantibodies can prolong COVID-19 symptoms. Their 2022 study involved 34 participants experiencing long COVID, and 15 who had recovered. The focus was on immunoglobulin G (IgG) antibodies, which were administered to mice.</p>

<p>Mice injected with IgG from long COVID patients displayed heightened sensitivity to touch and pain, removing their paws from hot surfaces more quickly than those who received antibodies from non-long COVID participants. Eikelkamp noted that this aligns with symptoms reported by long COVID patients.</p>
<p>In 2024, the team repeated the experiment with IgG from 19 long COVID patients, confirming similar results. "These autoantibodies persist in the patient’s body," comments <a href="https://www.unamur.be/en/profil/nicaisec">Charles Nicaise</a>, who participated in another study from the University of Namur, Belgium.</p>
<p>This aligns with findings from three other preliminary studies. One led by <a href="https://medicine.yale.edu/profile/akiko-iwasaki/">Akiko Iwasaki</a> at Yale University found elevated autoantibody levels in patients with both long COVID and neurological symptoms. Mice injected with these antibodies also exhibited similar pain and balance issues.</p>
<p>The two remaining studies, published in November 2025, found that mice injected with IgG from long COVID patients demonstrated decreased skin nerve fiber density, indicating nerve damage, and heightened sensitivity to cold and touch.</p>

<p>Ongoing research by Nicaise's team has found that IgG from long COVID patients leads to increased pain sensitivity in mice, with IgG accumulating around neurons involved in relaying sensory information, especially pain.</p>
<p>To transform these findings into effective treatments, it's crucial to identify which specific types of IgG are implicated in symptoms. Iwasaki's experiments have spotlighted two particular target proteins, MED20 and USP5.</p>
<p>Furthermore, it's essential to assess whether removing or inhibiting the activity of these autoantibodies alleviates symptoms. <a href="https://www.amsterdamumc.org/en/research/researchers/brent-appelman">Brent Appelman</a> from Eikelkamp’s team studies the effects of filtering these autoantibodies from patients' blood. While Eikelkamp acknowledges that apheresis isn’t a permanent solution—requiring hospital visits every few months—he views it as a promising proof of concept paving the way for more advanced medical therapies.</p>

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Source: www.newscientist.com

Ruxolitinib: Breakthrough Vitiligo Cream That Targets Immune Cells to Restore Skin Pigmentation

vitiligo skin pigmentation on female hands

Vitiligo results in paler, less pigmented skin patches.

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A groundbreaking cream targeting the underlying cause of vitiligo is set to be available through the UK’s National Health Service (NHS). In clinical trials, this cream significantly improved pigmentation in white skin patches associated with this condition. Despite previous controversies surrounding vitiligo treatment, it is important to note that vitiligo is neither painful nor dangerous.

“Typically, individuals with vitiligo exhibit no physical symptoms, but the condition can lead to significant psychological challenges,” stated David Rosmarin from Indiana University, who led two trials for the new ruxolitinib cream treatment.

The cream, already marketed in the United States under the name Opzelura, is indicated for treating non-segmental vitiligo, characterized by symmetrical white patches on both sides of the body. This condition is believed to result from the immune system mistakenly attacking melanocytes—the cells responsible for producing melanin, which gives skin its color.

According to Emma Rush from Vitiligo Support UK, this treatment represents the first rigorously tested medication that directly addresses the mechanisms causing vitiligo. “This is a significant milestone in vitiligo treatment,” she remarked.

Ruxolitinib functions by inhibiting the activity of enzymes that destroy melanocytes. While existing treatment options like steroid creams may restore some pigmentation, they have broader immune-suppressing effects.

A recent study published in 2022 revealed that ruxolitinib enhanced pigmentation and decreased the visibility of vitiligo patches compared to a placebo cream. The effects were noted irrespective of the individual’s skin color (vitiligo tends to be more conspicuous on darker skin tones), and these results were sustained for at least one year after treatment cessation for over a third of participants.

The National Institute for Health and Care Excellence (NICE) has previously reviewed the efficacy of ruxolitinib and concluded that it is not cost-effective for NHS provision. However, it is now recommended that this cream be available to individuals aged 12 and older with non-segmental vitiligo when other topical treatments have proven ineffective or unsuitable.

Vitiligo affects approximately 1% of the global population, with severity ranging from a few small patches to larger, inflamed, or discolored areas of skin.

“Patients and clinicians may sometimes believe that vitiligo does not require treatment since it is not life-threatening or physically painful,” noted Victoria Eleftheriadou of the British Association of Dermatologists. However, vitiligo can lead to serious complications, including depression and anxiety.

Natalie Umbersley, a vitiligo ambassador for the charity Changing Faces, stated that support groups encourage individuals with visible differences to seek treatment without fear of judgment but expressed her reluctance to pursue ruxolitinib after years of using existing therapies. “I have learned to embrace my unique skin,” she said. “It’s all about celebrating our individuality.”

“While it’s wonderful to have individuals who love their appearance, this is not the reality for everyone,” commented Rush.

While an oral form of ruxolitinib has been used to treat certain cancers and rheumatoid arthritis, it is associated with serious side effects such as lymphoma, heart disease, and infections. However, these risks are not reported with the topical formulation. In two vitiligo trials, ruxolitinib was linked to only mild side effects, including acne and itching. “Systemic absorption is minimal,” Eleftheriadou noted.

Ruxolitinib is also considered to be safer than long-term use of steroid creams, which can cause skin thinning. Additionally, ultraviolet light therapy may be an option for individuals with severe vitiligo, although it is not widely accessible.

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Source: www.newscientist.com

Tattoos May Impact Local Immune System Function

Some researchers are concerned that tattoos might be hazardous to health

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Research indicates that tattoo ink can accumulate in lymph nodes, potentially disrupting the immune system and leading to permanent alterations in the body’s disease defense mechanisms.

This conclusion arises from a study involving mice, which revealed chronic inflammation in the lymph nodes of tattooed animals—nodes that were stained with ink—and modified antibody responses to vaccinations. Similarly, studies have shown inflammation and discoloration in the lymph nodes of individuals with tattoos, persisting for years after the tattoo was applied.

The findings suggest that tattoos could increase disease risk and highlight the necessity for further investigation. Santiago González from the University of Lugano, Switzerland, asserts, “When you get a tattoo, you are essentially injecting ink into your body. This affects not only the skin’s appearance but also the immune system. Chronic inflammation, over time, can deplete the immune system, increasing susceptibility to infections and certain cancers—many questions remain that require additional research.”

Tattoos are becoming increasingly popular worldwide, with approximately 30 to 40 percent of individuals in Europe and the United States sporting at least one tattoo. Though Gonzalez does not have a tattoo, he admires them as an art form, stating, “I think they’re visually appealing.” Nonetheless, the long-term health implications of tattooing—particularly concerning the immune system—are still not well understood.

Gonzalez noted that he and his team were conducting an unrelated investigation into inflammation in mice when they observed a “crazy inflammatory response” after applying small identifying tattoos. Curious, they decided to delve deeper.

The team utilized standard commercial inks in black, red, and green to mark 25 square millimeter patches on the hind legs of several mice. With specialized imaging technologies, they tracked the ink traveling through lymph vessels towards nearby lymph nodes almost immediately, often within minutes.

In these nodes, the researchers found that macrophages (immune cells that eliminate debris, pathogens, and dead cells) absorbed the ink, turned the nodes discolored, and initiated acute inflammation. Within approximately 24 hours, these macrophages would perish and release the ink, which would then be taken up by other macrophages, creating a continuous cycle of chronic inflammation that outlasted the healing of the tattoo site.

After two months, during which the tattoos remained, the mice still exhibited inflammatory markers in their lymph nodes that were up to five times higher than typical, Gonzalez reported.

To comprehend how this inflammation affected immune functioning, the researchers administered a vaccine directly into the tattooed skin. Notably, the tattooed mice demonstrated a markedly weaker antibody response to the COVID-19 mRNA vaccine compared to control mice, while showing a stronger response to the influenza vaccine.

Further analysis revealed that the lymph node macrophages from tattooed mice were filled with ink and struggled to capture the COVID-19 vaccine. For mRNA vaccines to be effective, they must be processed by macrophages. Conversely, the protein-based influenza vaccines triggered an enhanced antibody response, likely due to an increase in immune cells drawn to the tattoo site. “The response may vary based on the type of vaccine,” Gonzalez explained.

Lastly, the researchers investigated a limited number of lymph node biopsies from individuals who had tattoos near their lymph nodes. Two years post-tattoo application, the lymph nodes retained visible pigment, housed within the same type of macrophages observed in the mouse research. “Their lymph nodes were entirely filled with ink,” noted Gonzalez.

Crucially, he emphasized that even if individuals undergo tattoo removal, the ink is likely to persist in the lymph nodes for a lifetime. “You can eliminate ink from your skin, but the ink in your lymph nodes remains,” he stated.

The research findings illuminate the long-suspected link between tattoos and immune response. Christel Nielsen at Lund University, Sweden, indicated that her team had recently published findings that suggest individuals with tattoos have a heightened melanoma risk. She believes that the findings from Gonzalez’s team may be explained by increased inflammation in lymph nodes. “This study provides compelling proof that this is indeed the case,” she remarked, calling it a significant advancement in our understanding of the relationship between tattoos and disease.

For Michael Jurbdazian, this study conducted at the German Federal Institute for Risk Assessment in Berlin paints a clearer picture of how tattoo pigments interact with the immune system. However, he notes that results from mouse studies might not precisely mirror human outcomes, especially considering the differences between human and mouse skin. “The correlation with human health, particularly once healing is complete, necessitates more investigation,” he stated.

topic:

  • immune system/
  • inflammation

Source: www.newscientist.com

Breastfeeding Triggers Immune Cell Surge and May Offer Cancer Protection

Immune-related changes occur in the breast after breastfeeding

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Breastfeeding has long been linked to lowering the risk of breast cancer. However, the precise mechanisms behind this effect remain elusive. Recent studies reveal that women who breastfeed possess a higher presence of specialized immune cells in their breasts that might inhibit malignant immune cells.

Previous findings indicate that the risk of breast cancer, which is the second most prevalent cancer globally, decreases by 4.3% for each year of breastfeeding. This preventive effect appears to be particularly advantageous for older mothers.

The exact reasons remain partially understood, but are believed to involve alterations in breast tissue and hormonal exposure. To investigate further, Shereen Roy and colleagues at the Peter McCallum Cancer Center in Victoria, Australia, examined breast tissue from 260 women from diverse ethnic backgrounds, aged 20 to 70. These women varied in their maternal status and breastfeeding experiences, with none having previously been diagnosed with breast cancer.

“We discovered that breastfeeding mothers have a greater quantity of specialized immune cells known as CD8+ T cells, which can persist in breast tissue for decades after childbirth,” says Roy. “These cells serve as local defenders, poised to combat abnormal cells that may lead to cancer.” In certain instances, these cells remained present for up to 50 years.

The researchers also investigated mice, some of which underwent a complete cycle of pregnancy, lactation, and breast recovery during the weaning of their pups. Their mammary tissue was analyzed 28 days later, by which point the mammary glands had reverted to their pre-pregnancy state. Other mice had their pups taken away shortly after birth, or they were not pregnant at all.

The study revealed that completing a full lactation cycle significantly increased the accumulation of specialized T cells in mammary tissue, a phenomenon not observed in the other mice. When triple-negative breast cancer cells, known for their aggressive nature, were transplanted into the mammary gland tissue, tumors developed much more slowly in mice that had experienced lactation. However, depleting these T cells led to rapid tumor growth.

The researchers also analyzed clinical data from over 1,000 women diagnosed with triple-negative breast cancer post at least one full-term pregnancy. They found that women who breastfed exhibited tumors with a higher density of CD8+ T cells. “This indicates that the body’s immune response against breast cancer is active and ongoing,” notes Roy.

After considering other risk factors linked to breast cancer mortality, such as age, the researchers noted that women who breastfed had substantially longer overall survival. However, the variability in the data made it challenging to determine whether the duration of breastfeeding impacted this outcome.

The research team believes that T cells accumulate during breastfeeding to fend off infections that can lead to mastitis. Additionally, the relationship between pregnancy and breast cancer is complex, with studies indicating the risk being mitigated primarily for pregnancies occurring at younger ages.

“These findings have significant implications for understanding why certain women possess a more inherent protection against aggressive breast cancer and how we might develop targeted prevention and treatment strategies in the future,” Roy explains. However, she emphasizes that the choice to breastfeed is personal, not feasible for everyone, and may not always prevent breast cancer development.

Daniel Gray, along with researchers from the Walter and Eliza Hall Medical Research Institute in Victoria, highlighted that one of the study’s strengths was the analysis of multiple groups of women. “This lays the groundwork for future research that may elucidate how CD8+ T cells retain ‘memory’ of breastfeeding,” he comments.

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Source: www.newscientist.com

New mRNA Vaccine May Enhance Immune Response and Aid Cancer Survival

mRNA vaccines show growing potential to revolutionize healthcare

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The mRNA COVID-19 vaccination seems to offer an unexpected advantage: it may extend the lives of cancer patients by enhancing immunotherapy effectiveness.

A study analyzing about 1,000 individuals undergoing treatment for advanced skin and lung cancer revealed that those who received an mRNA COVID-19 vaccine within 100 days of starting treatment with an immune checkpoint inhibitor had nearly double the survival time compared to those who did not receive the vaccine during this period. Clinical trials to validate these findings are set to commence by year-end.

“The outcomes were astonishing,” states Elias Sayur, a researcher at the University of Florida. They speculate about the potential to develop an mRNA vaccine that enhances this immune response. “Could we craft a universal mRNA vaccine that activates the immune system across all cancer patients?” he muses. “The possibilities are extensive.”

However, is it advisable for someone just commencing checkpoint inhibitors to get a COVID-19 vaccine to improve treatment efficacy? “I am hesitant to provide clinical recommendations without concrete proof,” Sayur cautions. “Attempting to harness your immune system against cancer also carries risks,” he adds, urging adherence to established vaccine guidelines.

The rationale behind this finding lies in the immune system’s capacity to eliminate many cancers even before they escalate. Yet, some tumors evolve to obstruct this response. They achieve this by manipulating the “off switch” of T cells, which are responsible for destroying cancer cells. A well-known off switch is the protein PD-1 found on T cell surfaces.

PD-1 becomes inactive when it binds to a protein called PD-L1 on certain cell surfaces. This serves as a safety mechanism for cells to signal, “cease the attack, I am benign.”

Numerous cancers hijack PD-L1 by producing it in excessive amounts. Checkpoint inhibitors function by preventing PD-1 and other off switches from becoming activated. These treatments have significantly increased survival rates for conditions like lung cancer and melanoma, earning a Nobel Prize for their developers in 2018.

However, the efficacy of checkpoint inhibitors varies significantly. When an individual’s immune system fails to react to the tumor by dispatching T cells for an attack, these drugs offer limited benefit.

Consequently, combining checkpoint inhibitors with vaccines that bolster the immune system’s tumor combat capabilities could prove to be more effective than either strategy used in isolation. Cancer vaccines are generally tailored to elicit a response to mutated proteins in cancer cells and are often personalized. “We are attempting to discern the unique aspects of their tumors,” Sayur explains. “It demands substantial time, funding, and complexity.”

During cancer vaccine trials, his team observed that the non-specific mRNA vaccine used as a control also exhibited remarkable effectiveness. “It was an absolute surprise,” Sayur remarks.

In July, Sayur and colleagues published findings indicating that mRNA vaccines enhance anti-tumor responses, even when not aimed at cancer-specific proteins, as revealed in studies in mice. Vaccines can initiate an innate immune response that acts like an alarm, energizing the immune system and prompting T cells to move from tumors to lymph nodes, where they rally other immune cells for a focused attack.

Recognizing this potential, Sayur and his team examined the medical records of patients treated at the University of Texas MD Anderson Cancer Center.

Out of 884 advanced lung cancer patients receiving checkpoint inhibitors, 180 had received mRNA COVID-19 vaccinations within 100 days of initiating treatment. Those vaccinated survived for approximately 37 months, contrasting with roughly 20 months for those unvaccinated.

Furthermore, among 210 individuals with melanoma that had metastasized, 43 had been vaccinated within 100 days of starting checkpoint inhibitors. They had a survival time of around 30 to 40 months, compared to around 27 months for individuals who were not vaccinated in that time frame. Some vaccinated individuals remained alive at the time of analysis, indicating their survival may extend even longer. The research findings were shared at the European Society of Medical Oncology Congress in Berlin, Germany.

Previous reports have suggested that after receiving an mRNA COVID-19 vaccine, a proportion of tumors exhibited shrinkage, indicating potential anti-tumor effects in certain cases even without checkpoint inhibitors. “It’s certainly a possibility, but further investigations are essential to fully understand,” comments Sayur.

The United States recently declared significant cuts in funding for mRNA vaccine development, despite the substantial benefits they have provided during the pandemic and the vast potential they hold for treatments beyond vaccines.

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Source: www.newscientist.com

The Surprising Truth About Your Understanding of the Immune System

You may have come across the idea that high vitamin C intake can ward off colds, or perhaps TikTok nudged you to try turmeric or other supplements for immune support. The truth is, many of these strong claims and quick fixes are unfounded. There exists a myriad of myths surrounding immunity. Daniel Davis, an immunologist at Imperial College London, addresses these in his new book.

In Self-Defense: A Guide to Busting Myths About Immune Health, Davis aims to debunk these erroneous beliefs. He illustrates how advancements in technology, such as super-resolution microscopy, uncover the astonishing complexity of the immune system, illustrating how immune cells engage with their targets.

However, instead of feeling overwhelmed, he asserts that New Scientist shows us that this complexity can be empowering. It heightens our understanding of the immune system’s role in mental well-being, alerts us to lifestyle factors that might diminish immunity, and enhances our ability to distinguish between factual information and fads.

Helen Thomson: Let’s dive into the notion of “immune health” and the claims that it can be enhanced. That seems like a misleading concept, doesn’t it?

Daniel Davis: Absolutely. Many products claim they can “boost” immunity, but that’s a misleading notion. The immune system is not about simply enhancing your body’s infection-fighting capacity. Aggressive increases can inadvertently attack healthy cells, leading to autoimmune issues and allergies. A measured response is crucial.

So are we aiming to make our immune systems “smarter”?

Conventional discussions about immune health often lack subtlety. Each person’s immune system is wholly unique, shaped by genetics. Thus, when discussing immune health, we can only refer to what has been generally found to be effective: while general improvements may aid people, predicting individual outcomes is challenging.

Recent findings indicate that the immune system doesn’t operate in isolation; it’s influenced by diet, exercise, and the microbiome. Can we pinpoint which lifestyle factors significantly affect immune health?

The most substantial known influence on immune health is chronic stress. Regarding the other factors you mentioned, evidence exists, but causation is hard to prove. However, with stress, emerging molecular insights offer clarity on what occurs.

Which one in particular?

When the body detects a threat, it triggers a fight-or-flight response. The hypothalamus sends signals to the pituitary gland and adrenal glands, releasing cortisol and adrenaline. This prepares the body for action but quiets the immune response. For instance, short-term stress from parachuting only temporarily alters immune cell counts post-landing. However, sustained stress keeps cortisol levels elevated, which over time can undermine immunity, creating long-term challenges.

Orange juice is not the immune booster many believe

Marco Lissoni/Alamy

Our confidence in these findings stems from laboratory observations where elevated cortisol levels reduce the capacity of immune cells to eliminate virus-infected or cancerous cells. Coupled with observed correlations, such as individuals under long-term stress being less responsive to vaccines or more prone to infections, it’s evident that prolonged stress adversely impacts the immune system.

If you’re under stress and have adjusted your lifestyle, can your immunity be measured to see if these changes are effective?

It’s challenging to prove that lifestyle changes significantly mitigate long-term stress. While it’s a plausible assumption, demonstrating it empirically is difficult. Hospitals may track white blood cell counts as indicators of immune health, but given the vast range of immune cell types, simplifying measurements is a complex endeavor.

Experts, including well-known scientists, frequently claim that specific actions can bolster immunity. Should we take their word for it?

Consider orange juice as a prime example. During my upbringing, I believed that it was a cold remedy. However, that belief is misleading. This misconception stems from Linus Pauling, a two-time Nobel laureate famous for his work. In 1970, he published a bestseller entitled: Vitamin C and Colds, which inadvertently fueled a vitamin C craze based on selective data and anecdotal evidence, amplified by the media.


The most clearly proven effect on our immune health is long-term stress.

Interestingly, high doses of vitamin C do not determine whether you’ll catch a cold. While research shows that such supplementation can shorten the duration of colds by approximately 8%, this finding is tricky to interpret. Those taking high vitamin C might engage in other positive health behaviors that truly account for the shorter duration. Yet, this myth persists, rooted in the influential narratives of key scientists.

This history reminds us to remain cautious about individual anecdotes of success or insight. We need credible experts, but we should maintain a healthy skepticism towards singular opinions. Therefore, relying on established scientific consensus should guide us.

Lately, interest has surged surrounding the links between our immune systems, inflammation, and mental health. It’s a captivating area of research.

The relationship between the immune system and mental health is indeed a thrilling frontier. Initially, a group of individuals taking anti-inflammatory drugs for rheumatoid arthritis reported enhanced mental well-being prior to their physical improvements. These medications inhibit cytokine action, proteins produced by immune cells to facilitate communication.

Moreover, research indicates that individuals with certain mental health conditions exhibit elevated inflammatory markers in their blood. For instance, a study of nine-year-olds revealed that higher IL-6 cytokine levels predicted greater depression rates by age 18.

Animal studies present robust evidence as well. When injected with IL-6, animals demonstrated less exploratory behavior, paralleling signs of mental distress.

Yet, actionable strategies stemming from these insights remain elusive. Standard anti-inflammatory medications like aspirin or ibuprofen aren’t effective in treating depression, as several small trials have indicated. The question of whether anti-cytokine treatments can aid those with mental health issues remains unanswered, with current trials yielding inconclusive results.

Gut microbiome is important for a healthy immune system

Simone Alexowski/Science Photo Library

Future research should focus on identifying individuals who may benefit from interventions: Could individuals with particular mental health disorders who exhibit elevated cytokine levels and possibly other yet-undiscovered symptoms find relief through anti-cytokine therapies? While it’s a thought-provoking hypothesis, the journey to actionable solutions is ongoing. Understanding that your mental health may be linked to immune function can itself be empowering, marking a significant area of exploration.

People frequently ask how they can enhance their immunity. What do you tell them?

I have some insights, but they aren’t straightforward. Long-term stress is a concern. Getting adequate sleep is vital. However, individual needs can vary significantly. While I understand the importance of the microbiome, I can’t provide specific advice guaranteed to enhance it. These answers may disappoint, but embracing the complexity of the immune system is crucial. The lessons inherent in studying its intricacies are profound.

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Source: www.newscientist.com

Americans Awarded Nobel Prize in Medicine for Advancements in Understanding the Human Immune System

Three distinguished scientists (two from the U.S. and one from Japan) have been awarded the Nobel Prize in Medicine for their pivotal discovery related to peripheral immune resistance.

Mary E. Blankku, Fred Ramsdell, and Sakaguchi Shiko were jointly recognized for their breakthrough that “has invigorated the field of peripheral tolerance and contributed to the advancement of medical treatments for cancer and autoimmune disorders,” as stated in a news release by the Nobel Committee. The three recipients will share a prize of 11 million Swedish Kronor (approximately $1.2 million).

“This could also enhance the success rates of organ transplants. Several of these therapies are currently in clinical trials,” he noted.

Autoimmune diseases may arise when T cells, which serve as the body’s main defense against harmful pathogens, malfunction.

Their collective discovery establishes an essential foundation for understanding alternative methods by which the immune system, known as peripheral resistance, functions.

To mitigate damage, our bodies attempt to eliminate malfunctioning T cells within the thymus, a lymphoid organ, through a mechanism termed central resistance. Associated Press.

The groundbreaking research began in 1995 when Sakaguchi, a prominent professor at the Center for Immunology Frontier Research at Osaka University in Japan, uncovered a previously unknown class of immune cells that defend against autoimmune diseases.

Six years later, in 2001, Mary Blankku, who now serves as a senior program manager at the Institute of Systems Biology in Seattle, along with Ramsdell, a scientific advisor to Sonoma Biotherapeutics in San Francisco, identified a specific genetic mutation responsible for a severe autoimmune disease known as IPEX.

They designated this gene as foxp3.

By 2003, Sakaguchi confirmed that the FOXP3 gene he had identified nearly a decade prior was crucial for cell development. These cells are now referred to as regulatory T cells, which are essential in monitoring other T cells to prevent their malfunction.

“Their discoveries were vital for understanding the immune system’s functioning and why serious autoimmune diseases don’t affect everyone,” remarked All Kampe, Chairman of the Nobel Committee.

Nobel Committee Executive Director Thomas Perman announced the award on Monday morning, stating that he was only able to reach Sakaguchi.

“I hugged him in his lab, and he expressed immense gratitude, stating it was a tremendous honor. He was quite moved by the news,” Perman mentioned.

The awards ceremony is scheduled for December 10th, coinciding with the anniversary of Alfred Nobel’s death, a Swedish industrialist who founded the award to honor individuals who have significantly contributed to humanity. The inaugural award was revealed in 1901, marking the fifth anniversary of his passing.

The Nobel Prize in Physiology or Medicine will be announced in Stockholm at the Karolinska Institute on Monday, followed by the prizes for Physics, Chemistry, and Literature on the ensuing days.

The Nobel Peace Prize will be revealed on Friday.

Source: www.nbcnews.com

Nobel Prize in Medicine Awarded to Trio for Contributions to Immune Resistance

Mary Blankku, Fred Ramsdell, and Sato Shimajimajima have been announced as winners of the 2025 Nobel Prize in Physiology or Medicine by Committee Executive Director Thomas Perman.

Jonathan Nackstrand/AFP via Getty Images

The 2025 Nobel Prize in Physiology or Medicine has been awarded to three groundbreaking researchers: Mary Blank, Fred Ramsdel, and Shimon Sakaguchi. They have made significant discoveries regarding a unique type of immune cell that prevents the immune system from attacking its own body.

“We have opened up an entirely new area in immunology,” stated Marie Warren Hellenius from the Karolinska Institute in Sweden.

T cells, a type of immune cell, are crucial for detecting and neutralizing harmful viruses and bacteria. These cells are continuously produced throughout a person’s life.

At times, newly formed T cell receptors may mistakenly target the body’s own proteins instead of those from viruses or bacteria, resulting in autoimmune disorders like type 1 diabetes and rheumatoid arthritis.

The body possesses mechanisms to eliminate autoreactive T cells, with newly generated ones migrating to the thymus for evaluation. This has long been believed to be the sole process for the removal of self-targeting T cells.

Yet in 1995, Sakaguchi, now at Osaka University, demonstrated through a mouse study that other circulating cells in the bloodstream must provide some form of protection against autoreactive T cells. When the thymus is removed post-birth, mice develop autoimmune conditions; however, this outcome is averted when healthy T cells are introduced. His research identified that these particular T cells feature the CD25 protein on their surface, thereby classifying them as CD25-regulated T cells.

Meanwhile, Blankku, currently affiliated with the Institute of Systems Biology in Seattle, and Ramsdell, who advises Sonoma Bitherapeutics in San Francisco, studied mouse strains predisposed to autoimmune diseases. In 2001, Brunkow and Ramsdell identified that these mice possess mutations in a gene located on the X chromosome, specifically FOXP3.

Individuals with mutations in this gene are particularly susceptible to autoimmune disorders due to a condition known as IPEX syndrome. In 2003, Sakaguchi connected these findings, showing that the FOXP3 gene is integral to the development of the CD25-regulated cells his team had identified. Many researchers previously remained skeptical of Sakaguchi’s assertions, according to Warren Hellenius. However, the findings from Brunkow and Ramsdell solidified the case.

The discovery of regulatory T cells could pave the way for improved treatments across a variety of conditions. Increasing the presence of regulatory T cells may help mitigate autoimmune responses that lead to diseases like type 1 diabetes. Conversely, reducing these cells can amplify the immune system’s response against cancer. Numerous clinical trials are currently being conducted.

“Their discoveries have been fundamental in understanding the workings of the immune system and explaining why serious autoimmune diseases don’t universally develop,” remarked Orkenpe, the chairman of the Nobel Committee, in a statement.

Topics:

  • Immune system/
  • Nobel Prize

Source: www.newscientist.com

Balancing Immune Health and Chronic Inflammation: A Delicate Trade-off

The immune system may be even more intricate than we previously realized

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Having an adequately functioning immune system for extended lifespans might come with the trade-off of chronic inflammation. Some immune cells are programmed to undergo inflammatory deaths to protect against infections, but this can also happen randomly when no pathogens are present.

Our innate immune system comprises cell groups that react swiftly to invasive pathogens such as viruses and bacteria. These cells typically detect microorganisms when they invade or infect them.

“With minimal information such as molecules of viral DNA, immune cells can swiftly decide on a course of action, often opting for self-destruction,” says Randal Halfman from the University of Kansas Cancer Center.

This type of cell death, known as pyroptosis, is triggered by a double death domain protein. These proteins usually float within innate immune cells, but upon encountering pathogens, they assemble into crystal-like structures. This action activates another protein that kills the cells by creating holes, leading to ruptures and releasing inflammatory signals that assist the immune system in pathogen clearance.

To delve deeper into this process, Halfman and his team carried out various laboratory experiments investigating human death-fold domain proteins in yeast cells. This process allowed them to identify five types of these proteins with chemical characteristics that predispose them to naturally form crystal-like structures in the absence of pathogens. They then analyzed existing data to assess the levels of these proteins in uninfected human immune cells.

From this analysis, we determined that certain innate immune cells, such as macrophages that engulf and eliminate pathogens, possess five times more death-fold domain proteins at concentrations sufficient to spontaneously assemble and trigger cell death. “At high enough concentrates, these particles are more likely to randomly conform into crystal structures during the cell’s lifespan,” Halfman explains.

Such phenomena can accumulate with age, contributing to chronic inflammation associated with various conditions, including cancer and Alzheimer’s disease, according to Halfman. “It seems we’ve evolved this way to fend off infections, but it may also lead to chronic inflammation,” he asserts.

This pathway provides protection against infections from birth and enhances our likelihood of aging, though it might also predispose us to inflammation-related diseases later in life, Halfman notes. “If these persistent irritations continue over time, the resulting inflammatory damage can accumulate,” he elaborates. Andy Clark from the University of Birmingham, UK, agrees.

The development of medications that prevent spontaneous cell death could potentially alleviate chronic inflammation related to aging, Halfman suggests. However, Clark cautions that this might render individuals more vulnerable to infections.

topic:

  • Immune system/
  • inflammation

Source: www.newscientist.com

Cancer Cells Manipulate Immune Proteins to Evade Treatment – Sciworthy

Cancer arises from the proliferation of abnormal, uncontrolled cells that create dense masses, known as Solid Tumors. These cancer cells possess unique surface markers called antigens that can be identified by immune cells. A crucial component of our immune system, T cells, carry a protective protein known as FASL, which aids in destroying cancer cells. When T cells encounter cancer antigens, they become activated and initiate an attack on the tumor.

One form of immunotherapy, referred to as chimeric antigen receptor T cell therapy or CAR-T therapy, involves reprogramming a patient’s T cells to recognize cancer cell antigens. However, CAR-T therapy often struggles with solid tumors due to the dense, hostile environment within these tumors, which obstructs immune cells from infiltrating and functioning effectively.

Another significant hurdle that clinicians encounter when treating solid tumors is their heterogeneous composition of various cancer cell types. Some of these cells exhibit antigens recognizable by CAR-T cells, while others do not, complicating the design of CAR-T therapies that can target all tumor cells without harming healthy cells. Solid tumors also produce the protein Plasmin, which further impairs the immune system’s ability to break down FASL and eliminate cancer cells.

Researchers from the University of California, Davis investigated whether shielding FASL from plasmin could preserve its cancer-killing capabilities and enhance the efficacy of CAR-T therapy. They found that the human FASL protein contains a unique amino acid compared to other primates, making it more susceptible to degradation by plasmin. Their observations suggested that when FASL was cleaved, it lost its ability to kill tumor cells. However, after injecting an antibody that prevents plasmin from cleaving FASL, it remained intact and preserved its cancer-killing function.

Since directly studying cell behavior in the human body poses challenges, scientists culture tumor cells and cell lines in Petri dishes under controlled laboratory environments. To gain insights into plasmin’s role, the team examined ovarian cancer cell lines obtained from patients, discovering that CAR-T resistant cancer cells exhibited high plasmin activity.

They noted that combining ovarian cancer cells with elevated plasmin levels with normal cells displaying surface FASL diminished FASL levels in the normal cells. When they added FASL-protecting antibodies, CAR-T cells effectively eliminated not only the targeted cancer cells but also nearby cancer cells lacking the specific target antigen. These findings indicated that plasmin can cleave FASL in T cells and undermine CAR-T therapy, suggesting that safeguarding FASL may enhance CAR-T treatment’s effectiveness.

To assess whether tumor-generated plasmin can deactivate human FASL in more natural settings, researchers examined its function in live tumors within an active immune system. They implanted ovarian, mammary, and colorectal tumor cell lines from mice into genetically matched mice to elicit a natural immune response. When human FASL protein was directly injected into mouse tumors, the cancer cells remained intact. In contrast, injecting a drug that inhibits plasmin resulted in cancer cell death. Additionally, administering FASL-protecting antibodies also led to the elimination of cancer cells.

As a final experiment, the team aimed to determine whether activated T cells from the mice’s immune systems could penetrate the tumors and kill cancer cells. They implanted mice with both plasmin-positive and plasmin-negative tumors, treating both with drugs to enhance immune cell activity and boost FASL production.

They discovered that in tumors with low plasmin levels, mouse immune cells expressed high amounts of FASL on their surfaces, while in tumors with elevated plasmin levels, FASL was significantly reduced. Once again, injecting FASL-protected antibodies into these tumors increased FASL levels. The researchers concluded that plasmin can diminish the immune system’s ability to eliminate cancer cells by depleting FASL from immune cells.

In summary, the team found that tumors exploit plasmin to break down the protective protein FASL, evading immune system attacks. Based on their findings, they proposed that plasmin inhibitors or FASL-protected antibodies could augment the effectiveness of immunotherapy in treating cancer.


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Source: sciworthy.com

Life-Saving Treatments for Fatal Genetic Disorders Through Brain Immune Cell Replacement

Microglia are specialized immune cells in the brain

Science Photo Library/Alamy

The process of replacing immune cells in the brain halts the advancement of a rare and terminal brain disorder known as ALSP. This also paves the way for future clinical trials targeting other neurological ailments.

Extensive research indicates that impaired microglia—specialized immune cells within the brain—play a role in various neurological disorders, including Alzheimer’s disease and schizophrenia. The term ALSP stands for adult-onset leukoencephalopathy with axonal spheroids and pigmented glia, characterized by mutations in genes responsible for the survival of these cells, resulting in a reduced number of microglia and leading to progressive cognitive decline. Currently, no effective treatment exists for this fatal illness.

To address this, Bo Peng from Fudan University in China and his team employed a novel treatment called microglia replacement therapy. Prior experiments in rodents have shown that implanted stem cells—capable of developing into different cell types—can effectively replace microglia. However, it is necessary to first eliminate existing microglia in the brain to facilitate this. This can be achieved using drugs that target protein microglia.

Pursuing this avenue, Peng and his colleagues conducted initial tests on five mice with genetic mutations analogous to those associated with ALSP. As the mutations already impacted protein microglia, the researchers did not need to deplete these proteins with medication. Subsequently, they transplanted stem cells from healthy mice into the affected mice. Fourteen months later, treated mice exhibited approximately 85% more microglia in their brains compared to six untreated mice harboring the same mutation. Notably, these treated mice also demonstrated improvements in motor function and memory.

Encouraged by these promising findings, the researchers extended the treatment to eight individuals diagnosed with ALSP, using donor stem cells without preconditions. One year post-treatment, brain scans revealed minimal changes in participants compared to scans taken before the procedure. In contrast, four untreated individuals displayed significant brain deterioration and lesions over the same period. This implies that microglial replacement therapy effectively halted the progression of the disease.

At the study’s outset, all participants underwent cognitive assessments using a 30-point scale, where a decrease in score indicated cognitive decline. Reassessments a year later showed that, on average, scores remained stable for those who received the microglia replacements.

These results point to microglial replacement therapy being a potentially effective solution for ALSP. However, since this represents the inaugural human trial, “we remain unaware of any potential side effects,” comments Peng. “Given the rapidly progressive and lethal nature of this disease, prioritizing benefits over possible side effects might be crucial.”

Chris Bennett from the University of Pennsylvania cites the historical use of stem cell transplants for treating neurological disorders. “It has demonstrated effectiveness, particularly through microglia replacement,” he states. Recent FDA approvals for two similar therapies addressing other rare brain conditions further support this. “While prior studies may not have used this exact terminology, they effectively addressed similar conditions,” Bennett elaborates. “I’d describe this as a smart and innovative application of stem cell transplants. Nonetheless, microglia replacement therapy has been evolving for decades.”

Despite this, the results underscore the broader implications of microglial replacement therapy. Experts believe this strategy could one day address more prevalent brain disorders. For example, certain genetic mutations significantly heighten Alzheimer’s disease risk and affect microglial function. Replacing these malfunctioning cells with healthy human equivalents could offer a promising avenue for treatment.

Topics:

  • Neuroscience /
  • Immune System

Source: www.newscientist.com

The Role of Your Young Brain and Immune System in Longevity

All organs seem to be equally unimportant for longevity

westend61 gmbh / alamy

In the quest for a long life, it appears that not all organs hold equal significance. Research indicates that maintaining a youthful brain and immune system is crucial, overshadowing even the aging of the heart or lungs.

We already know that different organs age at varying rates, but the factors that most significantly affect lifespan remain elusive. Hamilton Sehawee from the Icahn School of Medicine at Mount Sinai, New York, leads this inquiry.

To explore this, his team assessed the levels of around 3,000 proteins in blood samples from over 44,000 participants aged between 40 and 70 years, all part of the UK Biobank Study.

Leveraging genetic data from earlier studies, the researchers mapped the locations of these proteins in the body, identifying several that were notably concentrated in 11 regions, including the immune system, brain, heart, liver, lungs, muscles, pancreas, kidneys, intestines, and adipose tissue. Elevated levels of these proteins suggest vital roles in the proper functioning of these organs and systems.

The team then employed machine learning models to estimate the ages of participants based on half of the data, developing distinct models for each of the 11 body areas. Generally, these predictions were consistent with the actual ages of the participants, although some models did occasionally overestimate or underestimate, supporting the notion that organs indeed age differently, according to Oh.

Using their trained model, the researchers predicted the organ and immune system ages of the other half of participants who were monitored for an average of 11 years after blood samples were taken.

They discovered that having even one organ showing signs of premature aging or an aging immune system correlated with a 1.5 to 3 times higher risk of death during follow-up, with the stakes increasing alongside the number of aging organs.

Interestingly, exceptions arose in cases where the heart and lungs appeared considerably younger than anticipated, which did not correlate with a lower mortality risk during the study period. However, possessing a youthful brain or immune system was associated with a roughly 40% reduction in death risk. These areas also intensified the overall risk reduction to 56%, particularly when both were young.

“The brain and immune system influence numerous other bodily functions, so it’s expected that their deterioration could significantly impact life expectancy,” remarked Alan Cohen from Columbia University in New York.

Nonetheless, Cohen cautions that protein markers may not entirely encapsulate the aging process. “There may be gaps in our understanding of the exact origins of these proteins. Certain organs may release their proteins into the bloodstream more readily than others, skewing perceptions of their importance,” he notes.

Moreover, further research involving a broader demographic that includes more ethnic and economically varied populations is necessary, as the current study participants were predominantly affluent individuals with European ancestry, according to Richard Shiou of King’s College London. Oh and his team are planning additional studies to explore this further.

Even if these findings hold true, concrete methods for curbing the aging processes in the brain and immune system remain elusive. Oh mentions that pinpointing aging markers in these areas could pave the way for medication targeting.

topic:

Source: www.newscientist.com

The Great Multivitamin Myth: How Pills Can Harm Your Immune System

The immune system is intricate, consisting of a vast network of cells, proteins, and organs that serve as the body’s primary defense against infections. Given its vital role, it’s essential to maintain its health.

So, how can you achieve that? Similar to other crucial bodily functions, numerous supplements and products claim to enhance your immune system’s performance. However, the reality is that your body may not require these so-called enhancements. In fact, it often functions best when left to its natural processes.

Misconceptions About Immune Boosting

The idea of vitamins that “boost” immunity can be quite misleading. In theory, the immune system is self-sufficient and operates optimally if you maintain a healthy lifestyle.

Moreover, “boosting” the immune system is a somewhat ambiguous notion. Simply increasing the quantity of immune cells or similar components in your body may not be beneficial and could potentially be harmful.

Consider your immune system as a finely tuned machine, operating at peak efficiency as long as it receives proper maintenance. Attempts to push this machine into overdrive may lead to overheating or malfunction.

The same principle applies to the immune system; an overstimulated immune response can inadvertently attack healthy cells, resulting in autoimmune disorders.

“The immune system can typically maintain its own balance. As long as you adhere to a relatively healthy lifestyle, no additional enhancement is necessary,” stated Dr. Bobby Cherayil, author of The Logic of Immunity, in an episode of BBC Science Focus.

“This includes a nutritious diet, sufficient sleep, regular physical activity, and avoiding harmful practices such as smoking or excessive alcohol consumption.”

Though a decline in lifestyle can affect our immune system, this deterioration is gradual, often requiring severe circumstances for visible infection to occur.

“A diet lacking essential nutrients or severe vitamin deficiencies can negatively impact your immune system, but such deficiencies are generally quite extreme.”

Risks Associated with Vitamin Supplements

If you maintain a healthy lifestyle—eating well, sleeping adequately, and exercising regularly—what risk is there in taking supplements aimed at enhancing your immune system?

Often, the risks are minimal, with the primary concern being the lack of effectiveness. The body can only absorb a certain amount of vitamins, and excess amounts typically pass through the body and are expelled in urine.

This applies mainly to water-soluble vitamins; however, vitamins A, D, E, and K do not leave the system so easily, and an excess can lead to toxicity. For instance, too much vitamin D can cause nausea, weakness, and may ultimately lead to bone and kidney pain if left untreated.

Many immune-boosting supplements are categorized as “multivitamins,” which encompass various vitamins and minerals in a single tablet or capsule.

A significant study associated multivitamins with a high rate of placebo effects. Research indicates no significant health statistics difference from a control group.

Clinical trials revealed no notable variation in mental or physical health outcomes between those taking multivitamins and those who were not. However, individuals consuming multivitamins often believe these products contribute positively to their health.

The danger is that individuals might assume multivitamins can substitute for other health-boosting practices, leading to neglect in other health areas such as maintaining a balanced diet.

Long-term effects of excessive vitamin intake remain less understood, with some studies suggesting a connection between multivitamin use and increased risk of cancer, heart failure, or cardiovascular issues.

Research indicates risk may increase with age. A study from the University of Minnesota found that among over 38,000 women aged 62 and older, those taking supplements had a 2.4% higher mortality risk.

This area of research continues to evolve, and not all studies reach such dire conclusions. For instance, another study found no significant correlation between multivitamin use and overall mortality rates.

Vitamins Have Their Place…for Some

For many, a healthy lifestyle is all that’s needed to keep the immune system in optimal condition. However, there are individuals with significant vitamin deficiencies that require attention.

Globally, over 2 billion people lack essential vitamins, and certain demographic groups may require additional support.

Vitamin supplements can be beneficial, particularly for older adults who struggle with chewing or swallowing. This is also true for pregnant individuals or those with digestive issues (always consult a healthcare professional).

Ultimately, the immune system remains a highly advanced, self-regulating entity. For the average person, it functions effectively on its own. Immune-boosting supplements may not pose significant risks, but they often result in “expensive urine.”


About Our Expert, Bobby Cherayil

Cherayil is an associate professor of Pediatrics at Harvard University and author of The Logic of Immunity. His research focuses on the immune system and its response to infection and inflammation.

Read More:

Source: www.sciencefocus.com

Daylight Boosts Immune System’s Infection-Fighting Power: Study Findings

In their recent study, scientist Christopher Hall and his team at the University of Auckland concentrated on neutrophils, a specific type of white blood cell significant for antibacterial defense.

yi du et al. We identified a photoresponsive endometrial timer that regulates time variations in antibacterial activity. Image credit: Summerstock.

The researchers employed zebrafish as a model organism due to its similar genetic composition to humans, and its capability of being raised with a transparent body, facilitating real-time observation of biological processes.

“Previous research has noted heightened immune responses in the morning during the initial stages of active fish,” Dr. Hall explained.

“I believe this reflects an evolutionary adaptation where the host is more vigilant during daylight, thus more prone to encounter bacterial infections.”

Nevertheless, the team aimed to determine how immune responses align with sunlight exposure.

The findings revealed that neutrophils have a circadian clock that activates during the day, boosting their bacterial-killing efficacy.

Most cells in our body maintain a circadian clock to synchronize with external time, thus regulating bodily functions.

Light plays a crucial role in resetting these circadian clocks.

“Given that neutrophils are the first immune cells to respond to inflammatory sites, our results carry significant implications for therapeutic advancements in many inflammatory diseases,” Dr. Hall remarked.

“This discovery opens avenues for developing drugs aimed at neutrophil circadian clocks to enhance our capability to fight infectious diseases.”

Study will be featured in the journal Scientific Immunology.

____

Lucia Yi du et al. 2025. Light-regulated circadian timers optimize the bactericidal function of neutrophils and enhance daytime immunity. Scientific Immunology 10 (107); doi: 10.1126/Sciimmunol.Adn3080

Source: www.sci.news

Potential long-term consequences of measles: immune system memory loss and encephalitis

Measles is not just a rash and fever.

The outbreak of the disease in West Texas has sent 29 people, most of them, to hospitals, as they continue to grow. Two people have died, including a six-year-old child.

It remains to be seen how many people have become ill in the outbreak. There have been at least 223 confirmed cases, but experts believe hundreds more people may have been infected since late January. As public health officials try to slow the spread of the highly contagious virus, some experts are worried about long-term complications.

Measles is different from other childhood viruses that come and go. In severe cases, it can cause pneumonia. According to the Centers for Disease Control and Prevention, approximately one in 1,000 patients develop encephalitis or encephalitis or encephalitis, with one or two deaths in 1,000 people.

This virus can wipe out the immune system, a complication known as “immune amnesia.”

When you get sick with a virus or bacteria, the immune system has the ability to form memories that can quickly recognize and respond to pathogens if they are encountered again.

Measles targets cells in the body, such as plasma cells and memory cells, and contains their immunological memory, and destroys some of them in the process.

“No one can escape this,” said Dr. Michael Mina, a vaccine expert and a former professor of epidemiology at the Harvard Chan School of Public Health.

In a 2019 survey, Mina and his team discovered that measles infections can be wrecked from anywhere 11% to 73% of human antibody stockpiledepends on how serious the infection is. This means that if people had 100 antibodies to Chicken Pox before they developed measles, they would be left at just 50 after measles infection, potentially catching them and getting sick.

Iwasakimon, professor of immunology at Yale University School of Medicine, said: You forget who the enemy is. ”

Virtually everyone who contracts measles weakens the immune system, but some are hit harder than others.

“There's no world where you get measles and it won't destroy some [immunity]He said. “The problem is that it will destroy enough to have clinical impact.”

In a previous study in 2015, Mina presumed that the virus was a virus before vaccination, when measles was common It may be related to half of childhood deaths due to infectionmainly from other diseases such as pneumonia, sepsis, diarrheal diseases, meningitis.

Researchers found that after measles infection, the immune system was suppressed almost immediately and remained intact for two to three years.

“Immune amnesia begins as soon as the virus replicates in them [memory] Cells,” Mina said.

The best protection against serious complications is the measles vaccine. Two doses of the vaccine are 97% effective in preventing infection.

What is “immune amnesia”?

Our bodies are constantly exposed to a variety of bacteria and viruses in our environment. Over time, our immune system learns to remember a particular intruder and can take action immediately if we find something that doesn't belong to our body.

“Children are in contact with all sorts of microorganisms, and most of those encounters have not led to illness,” said Dr. Adam Ratner, pediatrician and director of the Department of Pediatric Infectious Diseases at NYU Langone Health. “Children often recover and have memories, so if they see the same strain of the virus that causes diarrhea, they will be the second disease they are exposed to.”

With immune amnesia, he said that if people are exposed to strains of the same virus again, their bodies will act as if it was the first time they had it and they don&#39t have that robust protection.

This means that the measles virus can destroy the immunity that people have accumulated over time, such as pneumonia, colds, flu, bacteria, and more that can cause other pathogens.

Mina elicited a comparison with HIV, saying that the level of immunosuppression in severe measles infection can be compared to HIV that has not been treated for years. However, he warned that HIV affects various parts of the immune system, and that people&#39s immune systems can ultimately recover from measles.

How does measles destroy the immune system?

Highly contagious viruses can destroy long-lived plasma cells that are present in the bone marrow and are essential to the immune system. Cells are like factories that expel antibodies to protect us from intruders entering our bodies.

“It&#39s almost like bombing a sacred city,” Mina said.

Measles also targets cells in our body, called memory cells. This is a cell that remembers what intruders look like, allowing the immune system to quickly identify and fight them in the future.

When you breathe a virus, it is enveloped in cells called macrophages. Macrophages function as “trojan horses” to collect viruses in lymph nodes, Iwasaki said.

Once there, the virus can bind and destroy these memory cells, wiping away some of our built-in immunity in the process.

“one time [memory cells] As it is excluded, we basically no longer have any memory of those specific pathogens, so we are more susceptible to most infectious diseases that are unrelated to measles,” Iwasaki said.

Will the immune system recover?

The way your body begins to regain immune memory after being surrounded by measles is to be exposed to other viruses and bacteria, get sick again, and boost your immune system.

Such immunity can be relearned, but University of Pennsylvania immunologist John Welley says that while such immunity can be relearned, he is particularly susceptible to other infectious diseases.

“As every parent of a daycare child knows, if you&#39’re building a lot of immunity at the time, you’re suffering through it,” Welley said.

Mina relearned our immunity and compared it to why babies seem to get sick frequently.

“The illness a baby gets is not because the baby is more vulnerable, because they don&#39t have the same immunological memory set yet,” he said. “They have to spend several years accumulating it through exposure, which is kind of what people experience after measles.”

How Measles Causes Brain Inflammation

What&#39s even more frightening is an untreated measles complication called subacute sclerosing pan encephalitis (SSPE), a brain disease that can occur for more than a decade, which is fatal after someone recovers from an infection.

For poorly understood reasons, the measles virus can cause persistent infections and lead to brain damage, leading to cognitive decline, coma, and death.

Researchers believe that SSPE was once considered rare, but is more common than realization. a Review of measles cases in California From 1998 to 2015, SSPE cases were found to occur at a higher rate than expected among children who were not vaccinated.

Dr. Bessie Gibberge, a pediatric infectious disease expert at Northwest Medicine, said the disease is progressive and symptoms occur at normal stages.

“It can start with just a change in personality and a change in behavior,” she said. In children, it can be as subtle as worse performance in school.

The disease then progresses and can eventually lead to seizures and abnormal movements, Siebarghese said. Finally, parts of the brain that regulate vital signs such as breathing, heart rate, and blood pressure can be damaged and can lead to death.

There is no cure for this disease and is almost always fatal. Patients usually survive 1-3 years after diagnosis. In the US, there are usually four to five cases each year, which can be underestimated, says Ratner of Nyu Langone Health.

“It’s probably more common than we think because it’s not always diagnosed,” he said. “But as these outbreaks become more common, I think we will clearly see more cases of SSPE.”

Source: www.nbcnews.com

Debunking the Multivitamin Myth: How Pills May Hurt Your Immune System

The immune system is a complex network of cells, proteins, and organs that acts as the body’s last line of defense against infection. Maintaining a healthy immune system is crucial for overall well-being.

While there are numerous supplements and products available to boost immune function, it’s important to understand that the immune system is a well-regulated system that typically functions optimally when you lead a healthy lifestyle.

Misconceptions about increasing immunity

Boosting immunity may seem like a good idea in theory, but in reality, the immune system is equipped to function efficiently on its own with the right lifestyle habits.

Attempting to supercharge the immune system with supplements can have negative consequences, as excess immune cells can lead to autoimmune diseases and other health issues.

According to Dr. Bobby Cherail, an expert in immunology, living a healthy lifestyle through proper diet, exercise, and avoiding harmful habits is the best way to support the immune system.

It’s important to note that the immune system may weaken with poor lifestyle choices, but infections typically occur only in extreme cases of malnourishment or deficiency.

Potential risks of vitamin supplements

While vitamin supplements may seem like a harmless way to boost immunity, there are risks associated with overconsumption of certain vitamins, such as vitamin A, D, E, and K.

Excess water-soluble vitamins are generally excreted by the body, but fat-soluble vitamins can accumulate and lead to toxicity if consumed in excess.

Studies have shown that multivitamins may not provide significant health benefits and can lead to a false sense of security, causing individuals to neglect other aspects of their health.

Long-term use of multivitamins has been linked to an increased risk of certain health conditions, especially in older individuals.

Vitamins still play a role…for some people.

While a healthy lifestyle is typically sufficient for maintaining a strong immune system, certain individuals with vitamin deficiencies may benefit from supplements.

People with difficulty chewing, swallowing, pregnant women, and those with digestive issues may require additional vitamin support to maintain optimal health.

Ultimately, the immune system is a highly efficient self-regulator, and for most people, immune-boosting supplements may not offer significant benefits.


About our expert Bobby Shereyle

Dr. Bobby Cherail is an associate professor of pediatrics at Harvard University, specializing in immunology and the immune system’s response to infection and inflammation.

Read more:

Source: www.sciencefocus.com

Antibody treatment restores immune function in elderly mice

Antibodies are proteins that can target and attack specific cells.

Mirror Images/Alamy

An experimental treatment rejuvenates the immune systems of older mice and improves the animals’ ability to fight infections. If this treatment is effective in humans, it could reverse the age-related decline in immunity that makes older people more susceptible to illness.

These reductions may be due to changes in blood stem cells, which can develop into all types of blood cells, including important components of the immune system. As we age, a greater proportion of these stem cells tend to produce some immune cells than others. Jason Ross at Stanford University in California. This imbalance impairs the immune system’s ability to fight infection. It also promotes chronic inflammation, which accelerates aging and increases the risk of age-related diseases such as heart disease, cancer, and type 2 diabetes.

Ross and his colleagues have developed a treatment that uses antibodies, proteins that recognize and attack specific cells, to target these biased stem cells. Next, they tested the treatment on six mice aged 18 to 24 months. This is roughly equivalent to a human being between 56 and 70 years old.

One week after receiving the antibody injection, these abnormal stem cells in the mice had decreased by about 38 percent compared to six rodents of the same age who did not receive treatment. They also had significantly higher amounts of two types of white blood cells important for recognizing and fighting pathogens, and lower levels of inflammation.

“You can think of this as turning back the clock,” says Ross. “We are adjusting these percentages [immune] more similar cells [those of] A young adult mouse. ”

To test whether these changes result in a stronger immune system, the researchers vaccinated 17 older mice with a mouse virus. Nine of these mice had received antibody treatment eight weeks earlier. The researchers then infected rodents with the virus. After two weeks, the number of infected cells in the animals was measured and it was found that almost half of the treated mice (4 out of 9) had completely cleared the infection, compared to 1 out of 8 of the untreated mice. It turned out that there was only one.

Taken together, these findings demonstrate that antibody treatment rejuvenates the immune system of aged mice. Humans, like rodents, have more abnormal blood stem cells as they age, so a similar antibody treatment could also boost their immune systems, Ross said.

Such a possibility is still far away, robert signer at the University of California, San Diego. First, we need a better understanding of the potential side effects of treatments. In an accompanying article, Signer and his colleagues write: Yasar al-Fat KassResearchers, also at the University of California, San Diego, suggest that depletion of stem cells, even abnormal stem cells, may increase cancer risk. On the other hand, “if you have a better immune system, you’ll be better at investigating cancer, so we don’t know exactly what will happen yet,” Signer says.

Still, Ross says these findings are a promising advance in understanding age-related immune decline and how to reduce it.

Aging is the biggest risk factor for various diseases. “Rejuvenating or improving immune function in older adults could really help fight infectious diseases,” Signer says. “It may also have an impact on different types of chronic inflammatory diseases. That’s what’s so exciting here.”

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Source: www.newscientist.com

Immune cells exhibit greater independence than previously believed

New research reveals that immune cells can independently navigate complex environments by actively shaping chemical cues, a discovery with significant implications for understanding immune responses and cancer metastasis. have.

Immune cells exhibit a higher level of self-directed mobility than previously appreciated. InFLAMES researcher Jonah Alanko has shown that these cells are more than just passive reactors to surrounding chemical signals. Instead, they actively modify these signals and skillfully navigate complex environments through self-organization.

Directional cell movement is an essential and fundamental phenomenon of life. This is an important prerequisite for personal development, vascular remodeling, immune response, etc.

The research conducted by postdoctoral researcher Jonah Alanko focused on the migration and navigation of immune cells within the body. Chemokines, a type of signaling protein, play an important role in directing immune cells to specific locations. Chemokines, for example, form in lymph nodes and create chemical cues called chemokine gradients that cells in the body follow. According to Alanko, these chemokine gradients are like scent trails left in the air, getting brighter as you move away from their source.

The traditional idea was that immune cells recognize targets according to pre-existing chemokine gradients. In other words, cells that follow these cues have been viewed as passive actors, when in fact they are not.

Dendritic cells move through a microscopic maze with the help of chemokine gradients they create. In the upper image, the nucleus of the cell is drawn in blue, and the lines in the lower image represent the movement of the cell.Credit: Jonna Alanko, University of Turku

“Contrary to previous notions, we were able to demonstrate for the first time that immune cells do not need pre-existing chemokine gradients to find their way. They can create their own gradients, making complex We can move collectively and efficiently even in difficult environments,” Alanko explains.

cells consume chemokines

Immune cells have receptors that can sense chemokine signals. One of these receptors is called CCR7 and is present on dendritic cells.

Dendritic cells are specialized antigen-presenting cells that have a critical role in activating the overall immune response. We need to find the infection, recognize it, and then move to the lymph nodes with that information. In lymph nodes, dendritic cells interact with other cells of the immune system to mount an immune response against pathogens.

Alanko’s research showed that dendritic cells not only register chemokine signals at the CCR7 receptor, but also actively shape their chemical environment by consuming chemokines. The cells thereby create local gradients that guide their own movement and that of other immune cells. The researchers also discovered that another type of immune cell, her T cells, can benefit from these self-generated gradients to enhance their own directional movement.

“When immune cells are able to create chemokine gradients, they can guide the directional movement of themselves and other immune cells to avoid future obstacles in complex environments,” explains Jonah Alanko. do.

This discovery deepens our understanding of how immune responses are regulated in the body. But it can also reveal how cancer cells direct their movement to cause metastasis.

“The CCR7 receptor has also been found in many types of cancer, and in these cases this receptor has been shown to promote cancer metastasis. Cancer cells use the same mechanisms as immune cells to It may even guide its movement. Our findings therefore have the potential to help design new strategies not only to target specific cancers but also to modify immune responses. ,” said Jonah Alanco.

Reference: “CCR7 acts as both a sensor and a sink for CCL19 to coordinate collective migration of leukocytes” Jonna Alanko, Mehmet Can Uçar, Nikola Canigova, Julian Stopp, Jan Schwarz, Jack Merrin, Edouard Hannezo, Michael Sixt, September 1, 2023; scientific immunology.
DOI: 10.1126/sciimmunol.adc9584

Jonna Alanko is a postdoctoral researcher at the InFLAMES Flagship in the MediCity laboratory at the Faculty of Medicine, University of Turku, Finland. She carried out most of her recently published research in a research group led by Professor Michael Sixt at the Austrian Institute for Science and Technology (ISTA) in Austria.

Source: scitechdaily.com