Thymic function and peripheral T-cell homeostasis in rheumatoid arthritis.
T-cell diversity is generated through the production of new thymic emigrants. Thymic function declines with age, and the T-cell pool is maintained through homeostatic proliferation of naive peripheral T cells. This article discusses the impact of thymic output and peripheral T-cell homeostasis on the development of rheumatoid arthritis (RA). It is proposed that thymic output is prematurely compromised in RA patients. A compensatory expansion of peripheral T cells results in a contracted and distorted repertoire, possibly favoring T cells with autoreactive potential. Increased risk of autoimmunity, as a consequence of abnormal T-cell population dynamics, could be a common mechanism in chronic inflammatory diseases.
Goronzy
J J
JJ
Departments of Medicine and Immunology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA. goronzy.jorg@mayo.edu
Weyand
C M
CM
D000818:Animals; D001172:Arthritis, Rheumatoid / Q000209:etiology* / Q000276:immunology; D016922:Cellular Senescence; D002999:Clone Cells; D015329:Gene Rearrangement, T-Lymphocyte; D006706:Homeostasis / Q000276:immunology*; D006801:Humans; D051379:Mice; D018448:Models, Immunological; D013601:T-Lymphocytes / Q000276:immunology*; D013950:Thymus Gland / Q000166:cytology / Q000276:immunology*