Cited by 292T-cell and B-cell ImmunologyPsoriasis: Treatment and PathogenesisImmune Response and Inflammation

Immune aging and autoimmunity

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Goronzy, Jörg J., Weyand, Cornelia M.·2012·Cellular and Molecular Life Sciences

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.

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  • The incidence of autoimmune diseases increases in later life as the ageing immune system becomes unable to fully tolerate self-antigens.

    “The incidence of autoimmune diseases also increases in later life, as the ageing immune system becomes unable to fully tolerate self-antigens [19,37].”

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Authors
Goronzy, J. J., & Weyand, C. M.
Affiliations
Stanford Medicine (US)
Corresponding author
Goronzy, Jörg J.
Venue
Cellular and Molecular Life Sciences
Published
2012-04-01
Volume
69
Issue
10
Pages
1615-1623
ISSN
  • 1420-682X (ISSN-L)
  • 1420-9071
OpenAlex
W2072878467
Cited by
292
References
130
Citations by year
2026: 19 · 2025: 40 · 2024: 19 · 2023: 25 · 2022: 22 · 2021: 32 · 2020: 28 · 2019: 9 · 2018: 20 · 2017: 18 · 2016: 8 · 2015: 11 · 2014: 15 · 2013: 20 · 2012: 4
FWCI
1.48
Type
journal article
Language
en
Open access
Locations
  • Cellular and Molecular Life Sciences (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Heart, Lung, and Blood Institute (P01HL058000, R01HL117913)
  • National Eye Institute (R01EY011916)
  • National Institute of Allergy and Infectious Diseases (R01AI044142, R01AI108906, AI 90019, AI 57266, U19AI090019, U19AI057266)
  • National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR042527)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
immunosenescence, autoimmunity, autoimmune disease, T cell tolerance, autoantigens, neoantigens, memory-like T cells, lymphopenia, effector T cells, latent viruses, cytokine production, T cell homeostasis
MeSH terms
Age Factors, Aging, Autoimmune Diseases, Cell Differentiation, Humans, Immune Tolerance, T-Lymphocytes, Autoimmunity, Models, Immunological, Cell Proliferation

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