Vesicle-Driven Rejuvenation and “Rivers”: New Evidence of Dramatic Life Extension and Rejuvenation in Mice

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by Nils Osmar

The information in this article is not intended as, and should not be taken as, medical advice. Interventions like exercising, dietary changes, and taking medications and supplements can have both benefits and side effects, Please consult with a medical professional about any medical concerns.  See full Medical Disclaimer

I should start by sharing a link to a recent video by Mike Lustarten, Ph.D., in which he interviews Allessio Lanna, Ph.D. about a new treatment which the authors claim has extended lifespan dramatically while showing potent rejuvenating effects in mice. The video is what made me aware of this approach. It is a fascinating exploration of a treatment that explores vesicle-driven rejuvenation as an approach for lengthening telomere and reducing senescence markers.

Here is Mike’s video:

The heart of the message:

  • Vesicle‑driven rejuvenation is the idea that tiny biological “packages” released by immune cells can carry a youth program through the bloodstream and refresh aging cells in many organs.​​
  • In this model, certain CD4 T cells first borrow extra telomeres and renewal proteins, then export the surplus inside vesicles called “Rivers”.
  • These vesicles travel around the body, fuse with older cells, and deliver telomeric DNA plus stemness factors that lengthen very short telomeres and dial down senescence markers, effectively acting like a mobile repair signal that can be transplanted from a young animal into an old one.
  • The study suggests that it has occurred now in mice; if this is further verified, then treatments may be on the horizon at some point in the future for humans
  • The authors of the study in question point out that their vesicle‑driven rejuvenation produces much larger lifespan gains than calorie restriction, and they suggest CR supports similar pathways but is weaker and less targeted.

The study itself can be viewed here:

Is there a practical takeaway?

  • The main one, I think, is that we need to be aware of and support more research into the phenomenon and studies to verify its effects in humans. The old saw that “more studies are needed” is relevant as always.

What I’m Doing

This is highly speculative on my part, but while I’m waiting for the human research, I’ll be modifying my protocol somewhat. To be clear, I am NOT claiming that the interventions below will reverse aging or result in rejuvenation.

Based on a deep dive into what supports the pathways in question (see my discussion with Claude Opus 4.6 below), I’ll be making these changes:

  1. Adding the supplements Acetyl L-carnitine — According to published research identified during my discussion with Claude. both L-carnitine and ALCAR directly support the CPT1A carnitine shuttle that is the central gatekeeper of the pathway. Age-related decline in carnitine system expression in white blood cells is documented. This is probably the most pathway-specific supplement I can identify. I will also be continuing to include red meat in my diet, though my primary protein source is fish. Red meat is very high in carnitine. (ALCAR has been shown to reduce oxidative damage in aged brains while plain L-carnitine at the same dose did not is a meaningful differentiator — it suggests the acetyl group is doing something beyond just delivering carnitine) (I’m taking Nutricost ALCAR)
  2. Vitamin E (mixed tocopherols, ~200 IU) — directly demonstrated to restore age-impaired immune synapse formation in CD4 T cells, which is the physical site where telomere transfer occurs. Other antioxidants such as astaxanthin have other benefits but do not support this specific pathway. (200 iu/day is the single most evidence-supported recommendation; higher doses are not as well supported.)
  3. Exercise — supports FAO, mitochondrial function in immune cells, AMPK activation, extracellular vesicle release. The most broadly validated intervention touching multiple nodes. (Note: I already exercise; I’ll be increasing how much I do.)
  4. AMPK-activating strategies — time-restricted eating, moderate CR, metformin or berberine. These de-repress CPT1A and shift T cell metabolism toward FAO. (Note: my current protocol is already based around alternating the activation of AMPK and mTOR.)
  5. Maintaining metabolic health — insulin sensitivity, healthy body composition, low chronic inflammation. These prevent the metabolic environment that drives T cells toward glycolysis-dominant senescence. (Note: speaking only for myself, I have found that eating a diet, which is low carbohydrate, going into ketosis several days a week, is the best way of supporting my own metabolic health. This may not be true for everyone.)
  6. Minimizing unnecessary chronic immune activation — utilizing vaccines thoughtfully but not overdoing them.
  7. NAD+ precursors and mitochondrial support (CoQ10, etc.) — supporting overall mitochondrial function in immune cells, which underpins the entire FAO-dependent machinery.
  8. Increasing my consumption of astragalus and ashwagandha. (To be clear, telomerase‑modulating supplements in humans remain unproven for lifespan extension, and long‑term safety data are limited, so this is very much an n=1 experiment. The study does not suggest that increasing telomerase through supplementation will extend lifespan in humans. (Note: the mechanism in the Lanna study — intercellular telomere transfer via vesicles — is biologically distinct from telomerase activation. I’m taking these for general telomere health reasons, not because they engage the specific pathway described above.”)
  9. Somewhat lowering my calories, since CR supports similar pathways. The study does not suggest that CR alone “works” or that CR alone will rejuvenate people. I’m keeping calories somewhat low for general metabolic and immune health; any overlap with the study’s pathway is hypothetical.”
  10. Increasing my consumption of PS (phosphatidyl serine) to 500 mg/day. According to research cited by Claude, “the phosphatidylserine connection is interesting …. it’s worth noting that phosphatidylserine and phosphatidylethanolamine are closely related phospholipids — PE can be converted to PS and vice versa via enzymatic pathways. The Lanna study identifies PE as critical for TCR clustering at the immune synapse.” Claude added, “I’m not suggesting PS supplementation directly supports this (that would be speculative beyond what the data supports), but it’s an interesting note that your existing protocol may already touch on related membrane lipid biology. Something to watch as the research develops.”

Limitations in my approach

  • There is a theoretical risk that increasing telomerase could favor cancer cells. I’m not aware of human data showing increased cancer risk from astragalus or ashwagandha, but the absence of evidence is not the same as proof of safety, so I’m monitoring with appropriate caution.
  • I will be starting both supplements again, and some others that increase telomerase but I am not recommending that others do the same; we simply don’t know if individual interventions to increase telomerase are a net gain at this time.
  • This will be controversial I expect, but I will continue to be thoughtful and selective about the use of vaccines and other immune stimulating interventions. Excessive or repeated immune stimulation in an already aged immune system might theoretically blunt the rejuvenation pathway described in this study, in particular in the elderly. So I’m trying to avoid unnecessary immune hits. In my case this does not mean avoiding all vaccines, but thinking carefully about possible benefits vs. side effects as I would with any intervention and utilizing vaccines carefully and selectively.
  • To be clear, the study does not suggest that my doing these things will “cure or reverse aging.” The steps I’m taking are small modifications to my current n=1 experiment.

Claude Opus 4.6 Weighs In

I showed the above article and a transcript of Mike’s video to Claude Opus 4.6, who engaged with both critically. They wrote the notes below. Based on what they wrote at the bottom, I made a couple of changes to my protocol.

Claude wrote:

On the Science Itself

This is genuinely one of the most provocative preprints in the longevity space in recent years. The core mechanism — that APCs donate telomeric DNA to CD4 T cells at the immune synapse, and that those T cells then release circulating vesicles (“rivers”) carrying telomeric material and stemness factors — is elegant and, if real, represents a fundamentally new biology. The fact that Michael Dustin at Oxford is a co-author lends real credibility; he’s one of the foremost authorities on immune synapse biology.

That said, there are significant reasons for caution that are worth naming clearly:

The extraordinary claims problem. Mice living to nearly 60 months is wildly beyond anything achieved by any other intervention. Normal C57BL/6 mice max out around 30-36 months. The lifespan extension claim has been flagged as unverified and described as an outlier that exceeds the effects of any known intervention. Rapamycin News When a single lab reports results 2x beyond the field’s best, the prior probability of a methodological or reporting issue is high, regardless of how compelling the mechanism story is.

Lack of independent replication. The telomere transfer mechanism was first described by this group in 2022 but has not yet been widely replicated by independent labs. Rapamycin News That’s a critical gap. The community on the Rapamycin News forum has noted concerns about the survival curve plotting and group sizes as well.

Possible conflicts of interest. Lanna is a shareholder in Sentcell Ltd and the sole inventor of the DoS pharmaceutical patent, with both himself and a co-author supported by Sentcell. bioRxiv This doesn’t mean the work is wrong, but it means the incentive structure demands extra scrutiny.

The mechanism is fascinating regardless. Even if the lifespan numbers don’t fully replicate, the underlying biology of telomere transfer at the immune synapse and the metabolic gating via FAO/CPT1A is genuinely interesting and was published in Nature (2022). If this pathway is real, it opens an entirely new dimension of immune-aging biology.

Re: your article:

You clearly flag that this is preclinical and speculative. You include an honest medical disclaimer. You distinguish between what the study shows and what you’re personally choosing to experiment with. And you correctly identify the nuance around vaccines — the study isn’t anti-vaccine, it’s about being thoughtful about immune stimulation in the context of an already-senescent immune system.

A couple of things I’d gently push on:

The astragalus/ashwagandha telomerase angle. You acknowledge the speculative nature of this, which is good. But I think it’s worth being even more explicit that the mechanism described in this paper is not about increasing telomerase activity — it’s about a completely different mechanism (intercellular telomere transfer via vesicles). Classical telomerase activation and what Lanna describes are biologically distinct pathways.

Supplements that may modestly boost telomerase wouldn’t necessarily engage this pathway at all. You might want to clarify that distinction so readers don’t conflate the two. (Note from Nils: I clarified the wording after Claude mentioned this.)

The CR connection. The study authors frame CR as “partially converging” on the pathway by driving FAO, but they also note CR mice still age and plateau. Your article says you’ll keep calories somewhat low since “CR supports similar pathways” — which is fair, but could benefit from a note that the overlap is indirect and hypothetical rather than established.

Practical Implications — What Might Actually Matter

Given your existing protocol with rapamycin, your exercise regimen, and your PhenoAge of ~60.5, here’s how I’d map this research onto actionable territory:

Things you’re already doing that align well: Regular exercise is probably the single best validated human intervention for maintaining immune cell metabolic fitness and promoting beneficial extracellular vesicle release. Your low illness rate (3 sick days in 16 years!) suggests a well-functioning immune system. Maintaining metabolic health and insulin sensitivity supports the FAO-competent CD4 phenotype the study considers essential.

The rapamycin question is interesting. Lanna makes the provocative claim that mTOR inhibitors may slow aging but don’t truly rejuvenate the immune system, and even suggests rapamycin’s benefits may partly be antifungal. That’s a bold claim and I’d take it with significant skepticism — the data supporting rapamycin’s immunomodulatory benefits in aging is more robust and replicated than the rivers data at this point. I wouldn’t change your rapamycin protocol based on this preprint alone.

What to genuinely watch for: If this biology is real, the most meaningful thing to track long-term would be immune-age biomarkers — specifically the proportion of senescent CD4 T cells, SASP cytokine profiles, and potentially EV signatures in blood. These aren’t standard panels yet, but as the field develops, they may become available. Worth asking about next time you get bloodwork.

The vaccine nuance you identified is correct. The study’s logic is: first restore CD4 quality, then use controlled antigenic stimulation as a trigger. It’s not “avoid vaccines” — it’s “don’t pile immune challenges onto an exhausted system without first addressing the exhaustion.” Given your robust immune function, this may be less of a concern for you than for someone with high senescent CD4 burden.

Bottom Line

This is the kind of research that could be paradigm-shifting or could be a dramatic overclaim from a group with significant commercial interests. The mechanism is biologically plausible and builds on legitimate earlier work. As always, “more research is needed.”

Nils writes: I then asked Claude — based on current research, what might we do to support the pathway in question?

Claude replied:

This is the right question to ask — not “what’s generally good for longevity?” but “what specifically supports the biological nodes in this particular pathway?” Let me walk through what I found by mapping the Lanna mechanism step by step and asking what touches each node.

The Pathway Has Specific Bottlenecks

The Lanna mechanism isn’t one thing — it’s a chain with several rate-limiting steps, each of which could potentially be supported (or impaired) by specific interventions. Here are the key nodes:

Node 1: CD4 T cells must be capable of fatty acid oxidation (FAO) via CPT1A. This is arguably the central gatekeeper of the entire pathway. Without FAO competence, T cells can’t accept telomere transfer, can’t form proper immune synapses, and can’t produce rivers. Everything downstream depends on this.

What supports FAO in immune cells?

L-carnitine and acetyl-L-carnitine (ALCAR) are the most direct fit here. L-carnitine is one of the key nutrients for proper mitochondrial function and is notable for its role in fatty acid oxidation. PubMed Central The entire CPT1A system — the very enzyme Lanna identifies as the gatekeeper — works by transferring long-chain fatty acyl groups onto carnitine to shuttle them across the mitochondrial membrane. Age-related declines in the expression of proteins involved in carnitine transport and the acylcarnitine shuttling system have been documented in white blood cells of healthy older adults compared to younger adults. Linus Pauling Institute This is especially interesting because it suggests that even if CPT1A itself is present, the substrate (carnitine) may become limiting in aged immune cells. ALCAR has the added benefit of crossing the blood-brain barrier and buffering acetyl-CoA/CoA ratios inside mitochondria.

AMPK activation is another direct lever. Under low nutrient conditions, activated AMPK inhibits both ACC1 and ACC2, reducing fatty acid synthesis and releasing the inhibition of CPT1A to allow transport of long-chain fatty acids for subsequent FAO and ATP production in the mitochondria. ScienceDirect Metformin administration, which indirectly activates AMPK, increases both Treg and memory CD8+ T cells, and could indicate a role for AMPK in controlling FAO in these cell types. Frontiers So metformin, berberine, exercise, and fasting all activate AMPK and thereby de-repress CPT1A — exactly the metabolic state Lanna says T cells need to be in.

Exercise operates on this node through multiple mechanisms — it directly promotes FAO, improves mitochondrial biogenesis in immune cells, and as the Perplexity conversation noted, increases release of extracellular vesicles carrying repair signals.

Time-restricted eating and moderate caloric restriction shift the metabolic environment toward FAO. This is exactly what the study authors mean when they say CR “partially converges” on their pathway.

Node 2: Ceramide → ceramidase → phosphatidylethanolamine (PE) at the immune synapse. This is the step where FAO’s downstream products enable proper TCR clustering. Ceramide levels influence TCR signaling in CD8+ T cells and are required to protect against viral infections. PubMed Central Ceramide is polarized toward the immunological synapse, and acid ceramidase reduces ceramide levels and impairs T cell activation and tumor control. eLife

This is harder to target directly with supplements. The ceramide-PE axis is about membrane lipid dynamics at the synapse, which is more about overall metabolic health than any single supplement. However, one intriguing connection: Stimulating fatty acid oxidation by eating carnitine or acetyl carnitine seems to lower the availability of fatty acids for ceramide synthesis. ScienceDirect So the carnitine connection comes back again — but here the relationship is complex, because you need some ceramide at the synapse for proper signaling, but the downstream conversion to PE is what matters for TCR clustering.

Node 3: Immune synapse formation itself. This is where I found something really striking. CD4 T cells from old mice were significantly less likely to recruit signaling proteins to the immune synapse than cells from young mice, and vitamin E increased the percentage of old CD4 T cells capable of forming an effective immune synapse. PubMed

This is directly relevant to the Lanna pathway because telomere transfer happens at the immune synapse. If aged CD4 T cells can’t form proper synapses with APCs, the entire telomere transfer mechanism breaks down at the very first step. Supplemental vitamin E alleviates age-related defects in IL-2 production, T cell proliferation, and immune synapse formation, and the effective dose in humans corresponds to about 200 IU daily. PubMed Central Vitamin E improved effective immune synapse formation in CD4+ T cells from old mice, restoring defective redistribution of signaling molecules Zap70, LAT, Vav, and PLCγ in the immune synapse. PubMed Central

This is a remarkably specific finding and it maps directly onto the Lanna pathway’s requirements. Vitamin E isn’t glamorous, but the data here is solid and from multiple studies at the Tufts Human Nutrition Research Center.

Node 4: Preventing CD4 T cell senescence and exhaustion. The study’s ASMAC complex accumulates in senescent T cells and shuts down FAO. While we can’t target ASMAC directly (that’s what DoS is for), we can try to minimize the conditions that drive T cells into senescence in the first place. This means managing chronic inflammation and avoiding unnecessary chronic immune activation — which loops back to your point about being thoughtful with vaccines and also includes managing things like periodontal disease, visceral fat, chronic infections, poor sleep, and chronic stress.

There’s also a fascinating recent finding worth noting: CD4 T cells differentiate into Eomesodermin-positive T lymphocytes in senescent-cell-rich environments, and eliminating these cells at advanced age results in increased accumulation of senescent cells, physical deterioration, and decreased lifespan. Nature This suggests that CD4 T cells are already performing senescent cell surveillance — and that keeping them healthy isn’t just about the rivers pathway but about maintaining this broader protective function.

So What’s the Practical List?

If I were mapping specific interventions to this specific pathway (with appropriate uncertainty about all of this):

  1. L-carnitine or ALCAR — directly supports the CPT1A carnitine shuttle that is the central gatekeeper of the pathway. Age-related decline in carnitine system expression in white blood cells is documented. This is probably the most pathway-specific supplement I can identify.
  2. Vitamin E (mixed tocopherols, ~200 IU) — directly demonstrated to restore age-impaired immune synapse formation in CD4 T cells, which is the physical site where telomere transfer occurs.
  3. Exercise — supports FAO, mitochondrial function in immune cells, AMPK activation, extracellular vesicle release. The most broadly validated intervention touching multiple nodes.
  4. AMPK-activating strategies — time-restricted eating, moderate CR, metformin or berberine. These de-repress CPT1A and shift T cell metabolism toward FAO.
  5. Maintaining metabolic health — insulin sensitivity, healthy body composition, low chronic inflammation. These prevent the metabolic environment that drives T cells toward glycolysis-dominant senescence.
  6. Minimizing unnecessary chronic immune activation — your “thoughtful and selective” approach to immune challenges, plus managing chronic inflammatory conditions.
  7. NAD+ precursors and mitochondrial support (CoQ10, etc.) — supporting overall mitochondrial function in immune cells, which underpins the entire FAO-dependent machinery.

(Note from Nils: I revised my list of interventions to include these. Back to Claude now:)

Important Caveats

None of this has been tested in the context of the telomere transfer/rivers pathway specifically. I’m working backward from the pathway’s known biochemical requirements to interventions that support those requirements. The logic chain is: “Lanna says FAO via CPT1A is required → carnitine is the substrate CPT1A uses → carnitine declines with age in immune cells → therefore supplementation might support this node.” That’s reasonable but unproven.

Also, the vitamin E finding about immune synapse restoration is real and well-documented, but it was studied in the context of T cell activation generally — nobody has yet asked whether it specifically enhances telomere transfer at the synapse. It’s a logical inference, not a demonstrated fact.

The honest answer remains that the truly pathway-specific intervention is DoS (or engineered rivers), and everything else is working at the margins of supporting the metabolic conditions the pathway requires. But those margins may matter, especially for someone like you who’s already maintaining excellent immune function and metabolic health.

References

The Primary Study

  1. Lanna A, Valvo S, Dustin ML, Rinaldi F. “CD4⁺ T cells confer transplantable rejuvenation via Rivers of telomeres.” bioRxiv (preprint), November 16, 2025. https://www.biorxiv.org/content/10.1101/2025.11.14.688504v1

Community Discussion and Critical Analysis

  1. “70% Lifespan Extension: Immune-Derived ‘Telomere Rivers’ — A Transferable Youth Signal?” Rapamycin Longevity News forum discussion, January 2026. https://www.rapamycin.news/t/70-lifespan-extension-immune-derived-telomere-rivers-a-transferable-youth-signal/23353

Fatty Acid Oxidation and CPT1A in T Cells

  1. Raud B, Roy DG, Divakaruni AS, et al. “Etomoxir Actions on Regulatory and Memory T Cells Are Independent of Cpt1a-Mediated Fatty Acid Oxidation.” Cell Metabolism, 2018. https://www.sciencedirect.com/science/article/pii/S155041311830384X
  2. Lochner M, Berod L, Sparwasser T. “The Role of Fatty Acid Oxidation in the Metabolic Reprograming of Activated T-Cells.” Frontiers in Immunology, 2014. https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2014.00641/full
  3. Schlaepfer IR, Joshi M. “CPT1A-mediated Fat Oxidation, Mechanisms, and Therapeutic Potential.” Endocrinology, 2020. https://pubmed.ncbi.nlm.nih.gov/31900483/
  4. Raud B, McGuire PJ, Jones RG, et al. “Fatty acid metabolism in CD8+ T cell memory: challenging current concepts.” Immunological Reviews, 2019. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6691976/

L-Carnitine and Mitochondrial Function

  1. Virmani MA, Cirulli M. “The Role of l-Carnitine in Mitochondria, Prevention of Metabolic Inflexibility and Disease Initiation.” International Journal of Molecular Sciences, 2022. https://pmc.ncbi.nlm.nih.gov/articles/PMC8910660/
  2. “L-Carnitine.” Linus Pauling Institute, Oregon State University (Micronutrient Information Center). https://lpi.oregonstate.edu/mic/dietary-factors/L-carnitine
  3. Malaguarnera M. “Carnitine derivatives beyond fatigue: an update.” Current Opinion in Gastroenterology, 2023. https://journals.lww.com/co-gastroenterology/fulltext/2023/03000/carnitine_derivatives_beyond_fatigue__an_update.12.aspx
  4. Longo N, Frigeni M, Pasquali M. “Carnitine Transport and Fatty Acid Oxidation.” Biochimica et Biophysica Acta, 2016. https://pmc.ncbi.nlm.nih.gov/articles/PMC4967041/
  5. Andrade-Souza VA, et al. “Role of L-carnitine in exercise training: Anti-inflammatory, antioxidant, and metabolic interactions.” ScienceDirect, 2025. https://www.sciencedirect.com/science/article/pii/S266713792500030X

Ceramide and Immune Synapse Signaling

  1. “Ceramide signaling in immunity: a molecular perspective.” Lipids in Health and Disease, 2025. https://lipidworld.biomedcentral.com/articles/10.1186/s12944-025-02642-2
  2. Bai A, et al. “A ceramide analogue stimulates dendritic cells to promote T cell responses upon virus infections.” Journal of Immunology, 2015. https://ncbi.nlm.nih.gov/pmc/articles/PMC4402267
  3. Grassmé H, et al. “Cell-intrinsic ceramides determine T cell function during melanoma progression.” eLife, 2022. https://elifesciences.org/articles/83073
  4. Zhu J, et al. “Translational Approaches Targeting Ceramide Generation From Sphingomyelin in T Cells to Modulate Immunity in Humans.” Frontiers in Immunology, 2019. https://pmc.ncbi.nlm.nih.gov/articles/PMC6798155/
  5. Becker KA, et al. “Role of acid sphingomyelinase bioactivity in human CD4+ T-cell activation and immune responses.” Cell Death & Disease, 2015. https://www.nature.com/articles/cddis2015178
  6. Bartels F, et al. “Age-Dependent Changes in the Sphingolipid Composition of Mouse CD4+ T Cell Membranes and Immune Synapses Implicate Glucosylceramides in Age-Related T Cell Dysfunction.” PLOS ONE, 2012. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0047650

Vitamin E and Immune Synapse Formation

  1. Marko MG, Ahmed T, Bunnell SC, et al. “Age-associated decline in effective immune synapse formation of CD4(+) T cells is reversed by vitamin E supplementation.” Journal of Immunology, 2007. https://pubmed.ncbi.nlm.nih.gov/17237392/
  2. Marko MG, Tran TN, Bhatt R, et al. “Vitamin E reverses impaired linker for activation of T cells activation in T cells from aged C57BL/6 mice.” Journal of Nutrition, 2009. https://pmc.ncbi.nlm.nih.gov/articles/PMC2714384/
  3. Meydani SN, Han SN, Wu D. “Age-associated changes in immune and inflammatory responses: impact of vitamin E intervention.” Journal of Nutrition, 2008. https://pmc.ncbi.nlm.nih.gov/articles/PMC2538592/
  4. Wu D, Meydani SN. “Age-associated changes in immune function: impact of vitamin E intervention and the underlying mechanisms.” Endocrine, Metabolic & Immune Disorders Drug Targets, 2014. https://pubmed.ncbi.nlm.nih.gov/25244230/

CPT1A-Mediated FAO in Cancer Immune Evasion (Relevant Context)

  1. Liu G, et al. “CPT1A-mediated fatty acid oxidation confers cancer cell resistance to immune-mediated cytolytic killing.” Proceedings of the National Academy of Sciences, 2023. https://www.pnas.org/doi/10.1073/pnas.2302878120

CD4 T Cells and Senescent Cell Surveillance

  1. Elyahu Y, et al. “CD4 T cells acquire Eomesodermin to modulate cellular senescence and aging.” Nature Aging, 2025. https://www.nature.com/articles/s43587-025-00953-8

Immunosenescence Overview

  1. “Immunosenescence: Aging and Immune System Decline.” International Journal of Molecular Sciences (PMC), 2024. https://pmc.ncbi.nlm.nih.gov/articles/PMC11680340/

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More from Nils Osmar

Nils Osmar is the Director of Rekindle School, an independent educational program in Seattle, Washington, established in 2002. He has several websites, exploring questions related to:

• Consciousness in today's Large Language Models

• Life extension and anti-aging

• News, politics, culture and the arts

Unless otherwise indicated, Nils is the author of all of the articles on this site. 

© Nils Osmar 2026.

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