Evidence map›Paper›PMID 35821833›Full record

ReviewFrontiers in aging2022

T-Cell Aging-Associated Phenotypes in Autoimmune Disease.

Tuantuan V Zhao, Yuki Sato, Jorg J Goronzy, Cornelia M Weyand

Abstract readReview
In one paragraph

Review in Frontiers in aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed.

  1. Review
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  7. Review
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  11. Review
  12. Article
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  14. Article
  15. Review
  16. Article
  17. T-Cell Senescence in Human Metabolic Diseases.Diabetes & metabolism journal · 2024
    Review
  18. Review
  19. Deciphering the aging process through single-cell cytometric technologies.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2024
    Review
  20. Immune checkpoints in autoimmune vasculitis.Best practice & research. Clinical rheumatology · 2024
    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.

Tuantuan V ZhaoMayo Clinic Alix School of Medicine, College of Medicine and Science, Rochester, MN, United States.
Yuki SatoMayo Clinic Alix School of Medicine, College of Medicine and Science, Rochester, MN, United States.
Jorg J GoronzyMayo Clinic Alix School of Medicine, College of Medicine and Science, Rochester, MN, United States.
Cornelia M WeyandMayo Clinic Alix School of Medicine, College of Medicine and Science, Rochester, MN, United States.

Funding

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
NHLBI NIH HHS R01 HL117913NHLBI NIH HHS R01 HL142068NIAID NIH HHS R01 AI108891NIAID NIH HHS R01 AI108906NIAID NIH HHS R01 AI129191NIAMS NIH HHS R01 AR042527NIA NIH HHS R01 AG045779
6 · The paper itself

Abstract

The aging process causes profound restructuring of the host immune system, typically associated with declining host protection against cancer and infection. In the case of T cells, aging leads to the accumulation of a diverse set of T-cell aging-associated phenotypes (TASP), some of which have been implicated in driving tissue inflammation in autoimmune diseases. T cell aging as a risk determinant for autoimmunity is exemplified in two classical autoimmune conditions: rheumatoid arthritis (RA), a disease predominantly affecting postmenopausal women, and giant cell arteritis (GCA), an inflammatory vasculopathy exclusively occurring during the 6th-9th decade of life. Pathogenic T cells in RA emerge as a consequence of premature immune aging. They have shortening and fragility of telomeric DNA ends and instability of mitochondrial DNA. As a result, they produce a distinct profile of metabolites, disproportionally expand their endoplasmic reticulum (ER) membranes and release excess amounts of pro-inflammatory effector cytokines. Characteristically, they are tissue invasive, activate the inflammasome and die a pyroptotic death. Patients with GCA expand pathogenic CD4

Indexed as

autoimmune diseasegiant cell arteritisimmune agingmitochondrial metabolismrheumatoid arthritistissue invasivenesstreg agingvasculitis

Identifiers

PMID35821833
PMCPMC9261367

What OpenQuestion holds

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Registered trials

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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.