Evidence map›Paper›PMID 40813808›Full record

ReviewNature aging2025

Aging reshapes the adaptive immune system from healer to saboteur.

Sandra Delgado-Pulido, Matthew J Yousefzadeh, Maria Mittelbrunn

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature aging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed.

  1. Article
  2. The immunology behind inflammaging-causes, sources, and mechanisms.The Journal of allergy and clinical immunology · 2026
    Review
  3. Review
  4. Review
  5. Article
  6. Gut · 2026
    Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Sandra Delgado-PulidoTissue and Organ Homeostasis Program, Centro de Biologia Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Madrid, Spain.ORCID http://orcid.org/0000-0003-2055-6594
Matthew J YousefzadehColumbia Center of Human Longevity, Columbia Center for Translational Immunology, Department of Medicine, Columbia University Irving Medical Center, New York, NY, USA. mjy2118@cumc.columbia.edu.ORCID http://orcid.org/0000-0003-2869-1029
Maria MittelbrunnTissue and Organ Homeostasis Program, Centro de Biologia Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Madrid, Spain. mmittelbrunn@cbm.csic.es.ORCID http://orcid.org/0000-0003-3487-8762

Funding

Investigating the Impact of Novel Senescent Microglia in Alzheimer's Disease ProgressionR21AG087361 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Yi Zhu · 2024 to 2026
$627k
Comunidad de Madrid PIPF-2022/SAL-GL-25208EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) ERC-2021-CoG 101044248-Let T BeU.S. Department of Health & Human Services | NIH | National Institute on Aging (U.S. National Institute on Aging) R21AG087361
6 · The paper itself

Abstract

The classical role of adaptive immunity as a protector against external threats has expanded to include its functions in cancer surveillance, tissue repair and regeneration, and, more recently, it has emerged as a regulator of the aging process. In this Perspective, we discuss the mechanisms by which the deterioration of adaptive immunity contributes to inflammaging, cellular senescence and age-associated pathologies. We propose that age-related changes in lymphocytes contribute to aging through two distinct mechanisms. First, adaptive immune function worsens with age, impairing immunosurveillance of damaged or senescent cells and diminishing tissue regenerative potential, thereby indirectly disrupting tissue homeostasis. This disruption is particularly important in the gut, where maintaining tissue and microbiota homeostasis is crucial for overall health during aging. Second, adaptive immune cells often acquire pro-inflammatory and autoaggressive phenotypes with age, directly driving tissue damage, promoting senescence and exacerbating inflammaging. Finally, we explore the therapeutic potential of strategies aimed at enhancing the protective functions of lymphocytes or modulating their pathogenic phenotypes to promote healthy aging.

Indexed as

Adaptive ImmunityAgingAnimalsCellular SenescenceGastrointestinal MicrobiomeHomeostasisHumansInflammationLymphocytes

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.