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Dairy cattle seem to survive infection with the H5N1 strain of influenza virus, which has killed millions of wild birds.Credit: Ben Brewer/Reuters
As the first-known outbreak of H5N1 avian influenza in cows continues in the United States, scientists are increasingly concerned that the animals will become a permanent reservoir for the virus, giving it more chances to mutate and jump to humans. Cows usually survive infection, which could make them a good place for viruses to acquire mutations by swapping genetic material — and there are a lot of cows. One dairy worker in Texas has definitely already been infected with H5N1 (with only mild symptoms) but there could be far more unidentified cases because testing of people is limited.
A new version of DeepMind’s AlphaFold tool gives scientists the ability to predict protein structures during interactions with other molecules. The tool could be transformative for drug discovery because it can predict the shape of proteins that contain function-altering modifications, or their structure alongside those of DNA, RNA and other cellular players that are crucial to a protein’s duties. “This is just revolutionary,” says biochemist Frank Uhlmann. “It’s going to democratize structural-biology research.” Access to the AlphaFold3 server, however, is limited — partly to protect the advantage of DeepMind’s own drug-discovery spin-off company.
The United States has introduced a new policy that provides stricter oversight of biological experiments that could be misused or spark a pandemic. It took more than four years of deliberations to develop a system that evaluates the risks and benefits of pathogen research without paralysing fundamental science. The policy, which comes into effect next year, sets a standard that might inspire other countries to re-evaluate their current approaches, says biosecurity researcher Filippa Lentzos.
Mexico has two scientist-candidates for president in its elections next month. Leading in the polls is environmental engineer Claudia Sheinbaum Pardo, who has vowed to “make Mexico a scientific and innovation power”. Sheinbaum Pardo would be the first woman and first environmental engineer to lead Mexico. Her rivals include computer engineer Xóchitl Gálvez Ruiz, who criticises Sheinbaum Pardo for not challenging current president Andrés Manuel López Obrador’s policies, including support for Mexico’s oil industry, a controversial science law and cuts to science spending. Some academics echo those concerns: “Is she going to continue López Obrador’s attacks on science or will she … radically change?” asks mathematician Raúl Rojas González.
Rejuvenating the immune system seems to revitalise many organs in an animal’s body — at least in mice. This raises the tantalising prospect of treating immune ageing to control age-related diseases. But interfering with the highly complex immune system can be perilous. Pioneers are setting their sights on low-risk but important goals, such as strengthening older people’s responses to vaccinations and boosting the efficiency of cancer immunotherapies.
In The Light Eaters, journalist Zoë Schlanger takes a deep dive into plant intelligence and consciousness — topics that were long considered pseudoscience. Some cautious studies have popped up, for example of a vine that changes the shape of its leaves to mimic those of neighbouring plants. “As a plant scientist, I am fascinated by what draws us to wanting to define plants as sentient or conscious — or not — through the lens of our limited human understanding of those terms,” writes reviewer Beronda Montgomery.
Do you have a work dilemma you’d like some help with? E-mail [email protected]
QUOTE OF THE DAY
In 2009, neuroscientist Larry Young wrote in Nature about his influential research into how the hormone oxytocin influences complex social behaviours such as the parent-infant bond and romantic love. Young has died, aged 56. (Nature | 5 min read)
Today, I want to share news of the Nature Awards Microbiome Accelerator for researchers with aspirations to translate their microbiome research to transform health outcomes. Four applicants will each receive US$10,000 and entry to an immersive residential programme. Learn more and apply here — the deadline is 24 June.
With contributions by Katrina Krämer, Smriti Mallapaty and Sarah Tomlin
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• Nature Briefing: Microbiology — the most abundant living entities on our planet — microorganisms — and the role they play in health, the environment and food systems.
Stem-cell researcher Carolina Florian didn’t trust what she was seeing. Her elderly laboratory mice were starting to look younger. They were more sprightly and their coats were sleeker. Yet all she had done was to briefly treat them — many weeks earlier — with a drug that corrected the organization of proteins inside a type of stem cell.
When technicians who were replicating her experiment in two other labs found the same thing, she started to feel more confident that the treatment was somehow rejuvenating the animals. In two papers, in 2020 and 2022, her team described how the approach extends the lifespan of mice and keeps them fit into old age1,2.
The target of Florian’s elixir is the immune system. The stem cells she treated are called haematopoietic, or blood, stem cells (HS cells), which give rise to all immune cells. As blood circulates, the mix of cells pervades every organ, affecting all bodily functions.
But the molecular composition of the HS cells changes with age, and this distorts the balance of immune cells that they produce. “Fixing the drift in them that occurs with time seems to fix a lot of the problems of ageing — not only in the immune system but also in the rest of the body,” says Florian, who is now at the Bellvitge Biomedical Research Institute in Barcelona, Spain.
In March3, another team showed that restoring the balance between two key types of immune cell gives old mice more youthful immune systems, improving the animals’ ability to respond to vaccines and to stave off viral infections.
How to make an old immune system young again
Other scientists have used different experimental approaches to draw the same conclusion: rejuvenating the immune system rejuvenates many organs in an animal’s body, at least in mice. And, most intriguingly, evidence suggests that immune-system ageing might actually drive the ageing of those organs.
The potential — helping people to remain healthy in their later years — is seductive. But translating this knowledge into the clinic will be challenging. Interfering with the highly complex immune system can be perilous, researchers warn. So, at first, pioneers are setting their sights on important yet low-risk goals such as improving older people’s responses to vaccinations and improving the efficiency of cancer immunotherapies.
“The prospect that reversing immune ageing may control age-related diseases is enticing,” says stem-cell scientist Vittorio Sebastiano at Stanford Medical School in California. “But we are moving forward cautiously.”
Fading immunity
The human immune system is a complex beast whose multitudinous cellular and molecular components work together to shape development, protect against infections, help wounds to heal and eliminate cells that threaten to become cancerous. But it becomes less effective as people age and the system’s composition starts to change. In older age, people become susceptible to a range of infectious and non-infectious diseases — and more resistant to the protective power of vaccines.
The immune system has two main components: a fast-acting innate system, which destroys invading pathogens indiscriminately, and a more-precise adaptive immune system, whose components learn to recognize specific foreign bacteria and viruses and generate antibodies against them.
The HS cells in the bone marrow spawn the immune cells of both arms of the system. They differentiate into two main classes — lymphoid and myeloid — which go on to differentiate further. Lymphoid cells are mostly responsible for adaptive immunity, and include: B cells, which produce antibodies; T cells, which help to attack invaders and orchestrate complex immune responses; and natural killer cells, which destroy infected cells. Myeloid cells include a raft of cell types involved mostly in innate immunity.
Proteins inside immune-cell-generating stem cells become more symmetrical with age (right).Credit: Eva Mejia-Ramirez
One of the earliest changes in the immune system as people age is the shrinking of the thymus, which begins after puberty. This organ is the crucible for T cells, but a lot of the tissue has turned to fat by the time people hit their 30s, slashing the production of new T cells and diminishing the power of the immune system. What’s more, the function of T cells alters as they age and become less specialized in their ability to recognize infectious agents.
The proportions of different types of immune cell circulating in the blood also changes. The ratio of myeloid to lymphoid cells skews markedly towards myeloid cells, which can drive inflammation. Moreover, increasing numbers of immune cells become senescent, meaning that they stop replicating but don’t die.
Any cell in the body can become senescent, typically when damaged by a mutation. Once in this state, cells start to secrete inflammatory signals, flagging themselves for destruction. This is an important anticancer and wound-healing mechanism that works well in youth. But when too much damage accumulates with ageing — and immune cells themselves also become senescent — the mechanism breaks down. Senescent immune cells, attracted by the inflammatory signals from senescent tissue, secrete their own inflammatory molecules. So not only do they fail to clean up properly, but they also add to the inflammation that damages surrounding healthy tissue. The phenomenon is known as ‘inflammaging’.
“It becomes a terrible positive feedback — a never-ending dance of destruction,” says immunologist Arne Akbar at University College London.
And evidence suggests that this feedback loop is kicked off by the immune system. In a series of experiments in mice4, Laura Niedernhofer at the University of Minnesota in Minneapolis has shown that immune-cell senescence actually drives senescence in other tissues. “These cells are extremely dangerous,” she says.
Her team used genetic methods to eliminate an important DNA-repair enzyme in the immune system of the mice. The animals remained healthy until adulthood but then, unable to correct accumulating mutations, various types of immune cell started to become senescent.
A few months later, increasing numbers of cells in organs such as the liver and kidney also fell into senescence, and the organs showed signs of damage. These effects were all reversed when the scientists gave the mice immune cells from the spleens of young, healthy mice.
All of this suggests that fixing the characteristics of immune-system ageing could help to prevent or mitigate diseases of ageing, says Niedernhofer.
Battling senescence
Many scientists are trying to do just that, from very different angles. Lots of the approaches hint that very short treatments of the immune system might have long-term effects, keeping side effects to a more manageable minimum.
One approach is to tackle senescent immune cells head on, using drugs to either remove them or block the inflammatory factors they secrete. “Senescent immune cells have long been known to be very modifiable in humans,” says Niedernhofer. “They go up if you smoke and down if you exercise.”
Are your organs ageing well? The blood holds clues
Some drugs — such as dasatinib, which is approved for the treatment of some cancers, and quercetin, which is marketed as an antioxidant dietary supplement but not approved as a drug — are known to reduce the age-related acceleration of senescence, and dozens of clinical trials are testing their impact on various age-related diseases. Niedernhofer herself is involved in a small clinical trial on older people with sepsis, a condition that becomes more deadly with age.
Her team is also doing experiments to assess which of the many types of immune cell is the most important in driving senescence in the body, which should help in the design of more precise therapies. Two types — T cells and natural killer cells — are emerging as key contenders, she says. She plans to screen natural products and drugs already approved for use by the US Food and Drug Administration for their ability to interact with those types of immune cell in senescence.
Akbar thinks that targeting inflammation itself might be as effective as targeting the senescent cells. He and his colleagues did a study in healthy volunteers using the investigational compound losmapimod, which blocks an enzyme involved in the production of inflammatory molecules called cytokines. They treated the volunteers with the drug for four days, and then, over the course of a week, measured their skin responses to an injection of the virus that causes chickenpox. Most people are exposed to this virus during their lives and it frequently lingers in the body. But with age, people tend to lose their immunity to it, and it can then manifest as shingles. The drug restored the immune response in the skin in older volunteers to a level similar to that seen in the younger volunteers5. In unpublished work, Akbar has found the same robust skin results up to three months later.
“Temporarily blocking inflammation in this way to allow the immune system to function might similarly boost the response of older patients to flu vaccinations,” says Akbar.
Immune boost
The value of priming the aged immune system before administering a vaccine has been demonstrated in a series of clinical trials led by researcher Joan Mannick, chief executive of Tornado Therapeutics, which is headquartered in Boston, Massachusetts. Those trials tested analogues of the drug rapamycin and other drugs with similar mechanisms, which target the immune system and are approved for prevention of organ transplant rejection and for the treatment of some cancers. The drugs block an enzyme, called mTOR, that is crucial for many physiological functions and which becomes dysregulated in old age.
For several weeks before receiving their influenza vaccinations, trial participants were treated with doses of the drugs that were low enough to avoid side effects. This treatment regimen improved their responses to the vaccine, and boosted the ability of their immune systems to resist viral infections in general.
Vaccines tend to work less efficiently in older adults, but new approaches could boost their power.Credit: Hector Vivas/Getty
But rapamycin can raise susceptibility to infection and affect metabolism, so Mannick is planning trials with similar drugs that might have a safer profile. “But there are all sorts of different ways to try to improve the immune system,” she notes.
One other way is to try to restore the function of the thymus to maintain the production of new T cells. Immunologist Jarrod Dudakov at the Fred Hutchinson Cancer Center in Seattle, Washington, is researching the basic biology of thymus cells to try to work out how they regenerate themselves after stressful assaults. “It’s all a bit early to see how this understanding will translate into the clinic,” he says. But he thinks that maintaining the ability of the thymus to generate a broad repertoire of T cells will be “foundational”.
Others are trying to combat ageing by generating thymic tissue from pluripotent stem cells for eventual transplantation. But Greg Fahy, chief scientific officer at Intervene Immune in Torrance, California, says he sees no need to wait for these long-term prospects to come to fruition, because an available drug — synthetic growth hormone — is already known to regenerate thymus tissue. He is doing a series of small studies on healthy volunteers using growth hormone as part of a cocktail of compounds. Early results indicate that the participants show increased levels of functional thymic tissue, and that their epigenetic clock — a biomarker of ageing — reverses by a couple of years6. Fahy is now extending the trial to look at whether the drug cocktail also improves physical fitness in a larger group of volunteers.
Turn back time
Another approach, not yet in the clinic, is to partially reprogram immune cells, to try to turn back the clock in cells that have become senescent. This involves transiently exposing the cells in a dish to a cocktail of transcription factors known to induce a pluripotent state in adult cells.
Reversal of biological clock restores vision in old mice
Sebastiano and his colleagues have shown in human cells that this process corrects the epigenetic changes that occur with ageing7. He has co-founded a start-up company to use the technique to try to counteract a problem in a cancer therapy known as CAR T, in which T cells are engineered outside the body to target and destroy a person’s cancer. But the T cells can turn senescent before they can be returned to the person. Rejuvenating them during the generation process would make production quicker and more robust, says Sebastiano.
Florian’s approach, too, aims to produce healthier immune cells — inside the body1,2. HS cells in the blood rack up epigenetic changes, and their environment also changes as they age. This causes proteins in the cells to arrange themselves more symmetrically — a process known as polarization — which shifts the balance of stem-cell differentiation in favour of myeloid cells over lymphoid cells. Florian’s studies used a four-day treatment with a compound, called CASIN, that inhibits one part of this process to correct the polarization, and helped the mice to live longer.
The team saw the same life-extending effects when HS cells from old mice given CASIN were transplanted into old mice that hadn’t received the treatment. “This very small step had a large impact,” says Florian.
Florian next hopes to bring her work to the clinic. As a first case study, she thinks her drug might support regeneration of the immune system after people receive chemotherapy for cancer.
How old?
Research on immune ageing faces some fundamental challenges. One is shared with ageing studies in all organs — the inability to measure ageing precisely.
“We don’t know in a quantitative, measurable, predictive way what ageing means at the molecular level in different cell types,” says Sebastiano. “Without those benchmarks, it is very hard to show rejuvenation.” Last year, a consortium of academics got together to begin developing a consensus on biomarkers of ageing — which will be essential when scientists come to seek approval from regulatory agencies for anti-ageing therapies.
Another challenge is the difficulty in pinning down what makes one immune cell unique. Until recently, it has been hard to demonstrate which subtypes of immune cells live where, and how they change with time.
But technologies such as single-cell RNA sequencing, which quantitatively measures the genes being expressed in individual cells, have tightened up analysis. A large study of immune cells in the blood of mice and humans across a range of ages published last November, for example, revealed 55 subpopulations. Just twelve of those changed with age8.
With so many strands of research coming together, scientists are cautiously hopeful that the immune system will indeed prove to be a key lever in healthy ageing. Don’t expect an elixir of youth any time soon, says Florian — by definition, ageing research takes a long time. “But there is such great potential for translation.”
A population of neurons in the brain stem, the stalk-like structure that connects the bulk of the brain to the spinal cord, acts as the master dial for the immune system.Credit: Voisin/Phanie/Science Photo Library
The results, published on 1 May in Nature1, suggest that the brain maintains a delicate balance between the molecular signals that promote inflammation and those that dampen it — a finding that could lead to treatments for autoimmune diseases and other conditions caused by an excessive immune response.
The discovery is akin to a black-swan event — unexpected but making perfect sense once revealed, says Ruslan Medzhitov, an immunologist at Yale University in New Haven, Connecticut. Scientists have known that the brainstem has many functions, such as controlling basic processes such as breathing. However, he adds, the study “shows that there is whole layer of biology that we haven’t even anticipated”.
The brain is watching
After sensing an intruder, the immune system unleashes a flood of immune cells and compounds that promote inflammation. This inflammatory response must be controlled with exquisite precision: if it’s too weak, the body is at greater risk of becoming infected; if it’s too strong, it can damage the body’s own tissues and organs.
Previous work has shown that the vagus nerve, a large network of nerve fibres that links the body with the brain, influences immune responses. However, the specific brain neurons that are activated by immune stimuli remained elusive, says Hao Jin, a neuroimmunologist at the US National Institute of Allergy and Infectious Diseases in Bethesda, Maryland, who led the work.
To investigate how the brain controls the body’s immune response, Jin and his colleagues monitored the activity of brain cells after injecting the abdomen of mice with bacterial compounds that trigger inflammation.
How the brain senses a flu infection — and orders the body to rest
The researchers identified neurons in the brainstem that switched on in response to the immune triggers. Activating these neurons with a drug reduced the levels of inflammatory molecules in the mice’s blood. Silencing the neurons led to an uncontrolled immune response, with the number of inflammatory molecules increasing by 300% compared with the levels observed in mice with functional brainstem neurons. These nerve cells act as “a rheostat in the brain that ensures that an inflammatory response is maintained within the appropriate levels”, says study co-author Charles Zuker, a neuroscientist at Columbia University in New York City.
Further experiments revealed two discrete groups of neurons in the vagus nerve: one that responds to pro-inflammatory immune molecules and another that responds to anti-inflammatory molecules. These neurons relay their signals to the brain, allowing it to monitor the immune response as it unfolds. In mice with conditions characterized by an excessive immune response, artificially activating the vagal neurons that carry anti-inflammatory signals diminished inflammation.
Dampening autoimmune symptoms
Finding ways to control this newly discovered body–brain network would offer an approach to fixing broken immune responses in various conditions such as autoimmune diseases and even long COVID, a debilitating syndrome that can persist for years after a SARS-CoV-2 infection, Jin says.
Cracking the genetic code of autoimmune disease
There’s evidence that therapies targeting the vagus nerve can treat diseases such as multiple sclerosis and rheumatoid arthritis, suggesting that targeting the specific vagal neurons that carry immune signals might work in people, Zuker says. But, he cautions, “it’s a lot of work to go from here to there”.
Besides the neuronal network identified in the study, there might be other routes through which the body transmits immune signals to the brain, says Stephen Liberles, a neuroscientist at Harvard Medical School in Boston, Massachusetts. What’s more, the mechanisms by which the brain sends signals back to the immune system to regulate inflammation remain unclear. “We’re just scratching the surface,” he says. “We need to understand the rule book of how the brain and the immune system interact.”
Blood stem cells (example pictured; artificially coloured) generate red blood cells and immune cells.Credit: Science Photo Library
Old mice developed more youthful immune systems after scientists reduced aberrant stem cells in the aged animals1. The technique strengthened the old rodents’ responses to viral infection and lowered signs of inflammation.
The approach, published on 27 March in Nature, treats older mice with antibodies to diminish a population of stem cells that give rise to a variety of other cell types, including those that contribute to inflammation. Excess inflammation can wreak havoc in the body, and these pro-inflammatory stem cells become dominant as mice and humans age.
It will be years before the approach can be tested in people, but many aspects of the stem-cell biology that underlies immune-cell production are similar between mice and humans. “It’s a really important first step,” says Robert Signer, a stem-cell biologist at the University of California, San Diego, who was not involved in the research. “I’m excited to see where they take this work next.”
Skewed immune system
For decades, researchers in Irv Weissman’s group at Stanford University in California have painstakingly tracked the fate of blood stem cells. These replenish the body’s stores of red blood cells (which carry oxygen from the lungs to all parts of the body) and white blood cells (which are key components of the immune system).
Pregnancy advances your ‘biological’ age — but giving birth turns it back
In 2005, Weissman and his colleagues found that populations of blood stem cells shift as mice age2. In young mice, there is a balance between two types of blood stem cell, each of which feeds into a different arm of the immune system. The ‘adaptive’ arm produces antibodies and T cells targeted to specific pathogens; the ‘innate’ arm produces broadbrush responses, such as inflammation, to infection.
In older mice, however, this balance becomes skewed towards the pro-inflammatory innate immune cells. Similar changes have been reported in the blood stem cells of older humans, and researchers speculate that this could lead to a diminished ability to mount new antibody and T-cell responses. That might explain why older people are more prone to serious infections from pathogens such as influenza viruses and SARS-CoV-2, and why they have weaker responses to vaccination than younger people do.
Restoring the balance
If that were the case, then restoring balance to the populations of blood stem cells could also rejuvenate the immune system. The team tested this by generating antibodies that bind to the blood stem cells that predominantly generate innate immune cells. They then infused these antibodies into older mice, hoping that the immune system would destroy the stem cells bound by the antibodies.
The antibody treatment rejuvenated the immune systems of the treated mice. They had a stronger reaction to vaccination, and were better able to fend off viral infection, than older mice who had not received the treatment. The treated mice also produced lower levels of proteins associated with inflammation than did old, untreated mice.
First hint that body’s ‘biological age’ can be reversed
This is an important demonstration that the different populations of blood stem cells influence how the immune system ages, says Signer.
But it’s also possible that the antibody treatment did more than just affect the dominant blood stem cell population, says Enca Montecino-Rodriguez, who studies the development of white blood cells at the David Geffen School of Medicine at the University of California, Los Angeles. The treatment might also affect the environment in which the blood stem cells live. Or it could clear other aged cells from the body, or trigger immune responses that affect how the mice respond to vaccines and viruses, she says.
Weissman says that his team is working on a similar approach to rebalance aged human blood stem cells. But even assuming ample funding and no unexpected setbacks, it will be at least three to five years before they can begin testing it in people, he says.
In the meantime, his team will continue to study mice to learn more about other effects of the antibody therapy, such as whether it affects the rates of cancer or inflammatory diseases. “The old versus the young blood-forming system makes a big deal of difference,” says Weissman. “It’s not just a difference in the bone marrow. It’s a difference all over the body.”
mRNA vaccines developed against the spike glycoprotein of severe acute respiratory syndrome type 2 coronavirus (SARS-CoV-2), displayed remarkable efficiency in combating coronavirus 19 (COVID-19). These vaccines work by triggering both cellular and humoral immune responses against the spike protein of the virus. Cellular immunity may play a more protective role than humoral immunity to variants of concerns (VOC) against SARS-CoV-2, as it targets the conserved regions of spike protein and possibly cross-reacts with other variants.
Since a single spike epitope is recognized by multiple T-cell clones, the mRNA vaccination-induced T-cell response may consist of multiple spike-reactive clones. Thus, it is important to understand the mechanism of mRNA vaccination-induced cellular immune response. However, to address this clonal-resolution analysis on T-cell responses to mRNA vaccination has not been performed yet.
To bridge this gap, a team of researchers, led by Associate Professor Satoshi Ueha, including Professor Kouji Matsushima from the Tokyo University of Science (TUS), Japan, Mr. Hiroyasu Aoki from the University of Tokyo, and Professor Toshihiro Ito from Nara Medical University, aimed to develop a kinetic profile of spike-reactive T-cell clones during repetitive mRNA vaccination. For this, they performed a longitudinal TCR sequencing on peripheral T cells of 38 participants who had received the Pfizer vaccine from before the vaccine to after the third vaccination and then analyzed the single-cell gene expression and epitope specificity of the clonotypes.
Their findings, published in Cell Reports on March 7, 2024, revealed that while the primary T-cell response of naïve T cells generally peaked 10-18 days after the first shot, expansion of “early responders” was detected on day 7 after the first shot, suggesting that these early responders contain memory T cells against common cold coronaviruses. They also found a “main responder” that expanded after the second shot and did not expand early after the first shot and a “third responder” that appeared and expanded only after the third shot.
By longitudinally tracking the total frequency of each response pattern, it was observed that, after the second shot, a shift among the clonotypes occurred, wherein the major population changed from early responders to main responders, suggestive of a shift in clonal dominance. A similar shift of responding clones was also observed in CD4+ T cells.
Expanding upon the research process, Prof. Ueha says, “We next analyzed the phenotype of main responders after the second and the third vaccination. The results showed that the main responders after the second and third shots mostly consist of effector-memory T cells (TEM), with more terminally differentiated effector memory-like phenotype after the third shot.”
The researchers then examined the repertoire changes of main responders, revealing that the expansion of main responders, which occurred after the second shot, diminished following the third shot, and the clonal diversity decreased and was partially replaced by the third responders. This may potentially mean that the third vaccination selected better-responding clones.
Due to the vaccination-induced shift in immunodominance of spike epitopes, the study supports the inter-epitope shift model. In addition, there were intra-epitope shifts of vaccine-responding clonotypes within spike epitopes.
Prof. Ueha explains the significance of these results, “Our analysis suggests that T cells can “re-write” themselves and reshape their memory populations after successive vaccinations. This re-writability not only maintains the number of memory T cells but also maintains diversity that can respond to different variants of pathogens. Moreover, by tuning the replacement of memory cells, more effective vaccines can be developed that can also be tailored to an individual’s unique immune response.”
Overall, this study provides important insights into mRNA vaccine-induced T-cell responses, which will be crucial for developing next-generation vaccines for more effective and broad protection against viruses.
