Evidence map›Paper›PMID 22466672›Full record

ReviewCellular and molecular life sciences : CMLS2012

Immune aging and autoimmunity.

Jörg J Goronzy, Cornelia M Weyand

Abstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 164 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
164citing papers in PubMed, 4 pooled it
6.2field-weighted citation impact, top 3% of its field
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

164 citing papers in PubMed, 4 syntheses or guidelines pooled it, 285 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. The efficacy and safety of immune checkpoint inhibitors in non-small cell lung cancer patients of different age groups: a meta-analysis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020
    Pooled it
  5. Trial
  6. Trial
  7. Review
  8. Age-associated Autoimmunity Driven by T cell Immunosenescence.bioRxiv : the preprint server for biology · 2026
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. How to measure and model cardiovascular aging.Cardiovascular research · 2025
    Review

104 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Jörg J GoronzyDivision of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, 269 Campus Drive West, Stanford, CA, 94305-5166, USA. jgoronzy@stanford.edu
Cornelia M Weyand
Stanford Medicine · USStanford University · US

Funding

VACCINE INDUCED IMMUNITY IN THE YOUNG AND AGEDU19AI057266 · NIAID · EMORY UNIVERSITY · PI Rafi Ahmed · 2003 to 2026
$81.7M
Vascular specific ACE expression and atherosclerosisP01HL058000 · NHLBI · VANDERBILT UNIVERSITY · PI DIKALOV, SERGEY · 1998 to 2013
$20.7M
Vaccination and infection: indicators of immunological health and responsivenessU19AI090019 · NIAID · STANFORD UNIVERSITY · PI DAVIS, MARK MORRIS · 2010 to 2015
$17.3M
The NOTCH Signaling Pathway in Large Vessel VasculitisR01HL117913 · NHLBI · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 2014 to 2025
$5.0M
Oligoclonal T Cell Expansion &Rheumatoid ArthritisR01AR042527 · NIAMS · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 1993 to 2022
$4.8M
Telomere Damage Responses and Immune AgingR01AI108906 · NIAID · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 2014 to 2024
$4.0M
CD8 T CELLS IN RHEUMATOID SYNOVITISR01AI044142 · NIAID · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 1999 to 2010
$2.9M
OCULAR DISEASE IN GIANT CELL ARTERITISR01EY011916 · NEI · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 1997 to 2011
$2.9M
NEI NIH HHS R01 EY011916NHLBI NIH HHS P01 HL058000NHLBI NIH HHS R01 HL117913NIAID NIH HHS AI 57266NIAID NIH HHS AI 90019NIAID NIH HHS R01 AI044142NIAID NIH HHS R01 AI108906NIAID NIH HHS U19 AI057266NIAID NIH HHS U19 AI090019NIAMS NIH HHS R01 AR042527
6 · The paper itself

Abstract

Age is an important risk for autoimmunity, and many autoimmune diseases preferentially occur in the second half of adulthood when immune competence has declined and thymic T cell generation has ceased. Many tolerance checkpoints have to fail for an autoimmune disease to develop, and several of those are susceptible to the immune aging process. Homeostatic T cell proliferation which is mainly responsible for T cell replenishment during adulthood can lead to the selection of T cells with increased affinity to self- or neoantigens and enhanced growth and survival properties. These cells can acquire a memory-like phenotype, in particular under lymphopenic conditions. Accumulation of end-differentiated effector T cells, either specific for self-antigen or for latent viruses, have a low activation threshold due to the expression of signaling and regulatory molecules and generate an inflammatory environment with their ability to be cytotoxic and to produce excessive amounts of cytokines and thereby inducing or amplifying autoimmune responses.

Indexed as

AutoimmunityModels, ImmunologicalAge FactorsAgingAutoimmune DiseasesCell DifferentiationCell ProliferationHumansImmune ToleranceT-Lymphocytes

Identifiers

PMID22466672
PMCPMC4277694
OpenAlexW2072878467

What OpenQuestion holds

Textmetadata
LicenceTDM
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.