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Arthritis Res Ther. 2003;5(5):225-34. Epub 2003 Aug 8.

Aging, autoimmunity and arthritis: T-cell senescence and contraction of T-cell repertoire diversity - catalysts of autoimmunity and chronic inflammation.

Author information

1
Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota, USA. goronzy.jorg@mayo.edu

Abstract

Rheumatoid arthritis (RA), like many other autoimmune syndromes, is a disease of adults, with the highest incidence rates reported in the elderly. The immune system undergoes profound changes with advancing age that are beginning to be understood and that need to be incorporated into the pathogenetic models of RA. The age-related decline in thymic function causes extensive remodeling of the T-cell system. Age-dependent changes in T-cell homeostasis are accelerated in patients with RA. The repertoire of naive and memory T cells is less diverse, possibly as a result of thymic insufficiency, and it is biased towards autoreactive cells. Presenescent T cells emerge that are resistant to apoptosis and that often expand to large clonal populations. These cells are under the regulatory control of nonconventional costimulatory molecules, display potent effector functions, and appear to be critical in the synovial and extra-articular manifestations of RA.

PMID:
12932282
PMCID:
PMC193735
DOI:
10.1186/ar974
[Indexed for MEDLINE]
Free PMC Article
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