期刊
FRONTIERS IN IMMUNOLOGY
卷 4, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2013.00131
关键词
immunosenescence; autoimmunity; inflammation; pathogenesis; DNA damage response; T cell receptor signaling; rheumatoid arthritis; giant cell arteritis
类别
资金
- US National Institutes of Health (NIH) [U19-AI057266, U19-A1090019, U01-AI089859]
- VA Merit award [BX001669]
- NIH [R01-AR042527, R01-AI44142, R01-EY011916, P01-HL058000]
- NATIONAL EYE INSTITUTE [R01EY011916] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL058000, R01HL117913] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R56AI044142, R01AI044142, R01AI108906, U19AI057266, U19AI090019, U01AI089859] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR042527] Funding Source: NIH RePORTER
- Veterans Affairs [I01BX001669] Funding Source: NIH RePORTER
Immune aging is best known for its immune defects that increase susceptibility to infections and reduce adaptive immune responses to vaccination. In parallel, the aged immune system is prone to autoimmune responses and many autoimmune diseases increase in incidence with age or are even preferentially encountered in the elderly. Why an immune system that suboptimally responds to exogenous antigen fails to maintain tolerance to self-antigens appears to be perplexing. In this review, we will discuss age-associated deviations in the immune repertoire and the regulation of signaling pathways that may shed light on this conundrum.
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