Evidence map›Paper›PMID 37542986›Full record

ReviewSeminars in immunology2023

Immune aging - A mechanism in autoimmune disease.

Yanyan Zheng, Qingxiang Liu, Jorg J Goronzy, Cornelia M Weyand

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
14.8field-weighted citation impact, top 1% 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

60 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
  2. Review
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  7. Article
  8. Immune responses in aging adults.The Journal of clinical investigation · 2026
    Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Immunoglobulin G in aging and cancer.Frontiers in immunology · 2026
    Review
  20. 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

4 authors at 2 institutions in 1 country.

Yanyan ZhengDepartment of Medicine, Mayo Clinic Alix School of Medicine, Rochester, MN 55905, USA; Department of Immunology, Mayo Clinic College of Medicine and Science, Rochester, MN, USA; Department of Cardiovascular Medicine, Mayo Clinic Alix School of Medicine, Rochester, MN, USA.
Qingxiang LiuDepartment of Medicine, Mayo Clinic Alix School of Medicine, Rochester, MN 55905, USA.
Jorg J GoronzyDepartment of Medicine, Mayo Clinic Alix School of Medicine, Rochester, MN 55905, USA; Department of Immunology, Mayo Clinic College of Medicine and Science, Rochester, MN, USA; Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.
Cornelia M WeyandDepartment of Medicine, Mayo Clinic Alix School of Medicine, Rochester, MN 55905, USA; Department of Immunology, Mayo Clinic College of Medicine and Science, Rochester, MN, USA; Department of Cardiovascular Medicine, Mayo Clinic Alix School of Medicine, Rochester, MN, USA; Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: Weyand.Cornelia@mayo.edu.
Mayo Clinic · USStanford University · US

Funding

VACCINE INDUCED IMMUNITY IN THE YOUNG AND AGEDU19AI057266 · NIAID · EMORY UNIVERSITY · PI Rafi Ahmed · 2003 to 2026
$81.7M
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
microRNA Regulation of T Cell SenescenceR01AI108891 · NIAID · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI GORONZY, JORG J · 2014 to 2023
$4.6M
Telomere Damage Responses and Immune AgingR01AI108906 · NIAID · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 2014 to 2024
$4.0M
Influence of Age on CD4 T Memory CellsR01AG045779 · NIA · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI GORONZY, JORG J · 2013 to 2023
$4.0M
T Cell Immunity in Giant Cell ArteritisR01HL142068 · NHLBI · STANFORD UNIVERSITY · PI Cornelia M. Weyand · 2018 to 2026
$3.3M
Memory T Cell Development and Survival in T Cell Responses of Older IndividualsR01AI129191 · NIAID · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI GORONZY, JORG J · 2017 to 2021
$1.9M
Mitochondrial Malfunction in T Cell Aging and Tissue InflammationU01AI179609 · NIAID · MAYO CLINIC ROCHESTER · PI Cornelia M. Weyand · 2024 to 2026
$1.7M
NHLBI NIH HHS R01 HL117913NHLBI NIH HHS R01 HL142068NIAID NIH HHS R01 AI108891NIAID NIH HHS R01 AI108906NIAID NIH HHS R01 AI129191NIAID NIH HHS U01 AI179609NIAID NIH HHS U19 AI057266NIAMS NIH HHS R01 AR042527NIA NIH HHS R01 AG045779
6 · The paper itself

Abstract

Evidence is emerging that the process of immune aging is a mechanism leading to autoimmunity. Over lifetime, the immune system adapts to profound changes in hematopoiesis and lymphogenesis, and progressively restructures in face of an ever-expanding exposome. Older adults fail to generate adequate immune responses against microbial infections and tumors, but accumulate aged T cells, B cells and myeloid cells. Age-associated B cells are highly efficient in autoantibody production. T-cell aging promotes the accrual of end-differentiated effector T cells with potent cytotoxic and pro-inflammatory abilities and myeloid cell aging supports a low grade, sterile and chronic inflammatory state (inflammaging). In pre-disposed individuals, immune aging can lead to frank autoimmune disease, manifesting with chronic inflammation and irreversible tissue damage. Emerging data support the concept that autoimmunity results from aging-induced failure of fundamental cellular processes in immune effector cells: genomic instability, loss of mitochondrial fitness, failing proteostasis, dwindling lysosomal degradation and inefficient autophagy. Here, we have reviewed the evidence that malfunctional mitochondria, disabled lysosomes and stressed endoplasmic reticula induce pathogenic T cells and macrophages that drive two autoimmune diseases, rheumatoid arthritis (RA) and giant cell arteritis (GCA). Recognizing immune aging as a risk factor for autoimmunity will open new avenues of immunomodulatory therapy, including the repair of malfunctioning mitochondria and lysosomes.

Indexed as

Arthritis, RheumatoidAutoimmune DiseasesAgedAgingCellular SenescenceHumansInflammationT-LymphocytesAutoimmune diseaseGiant cell arteritisImmune agingRheumatoid arthritisT cell aging

Identifiers

PMID37542986
PMCPMC10663095
OpenAlexW4385523118

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.