T-cell diversity is generated through the production of new thymic emigrant
s. Thymic function declines with age, and the T-cell pool is maintained thr
ough homeostatic proliferation of naive peripheral T cells. This article di
scusses the im pact of thymic output and peripheral T-cell homeostasis on t
he development of rheumatoid arthritis (RA). It is proposed that thymic out
put is prematurely compromised in RA patients. A compensatory expansion of
peripheral T cells results in a contracted and distorted repertoire, possib
ly favoring T cells with autoreactive potential. Increased risk of autoimmu
nity, as a consequence of abnormal T-cell population dynamics, could be a c
ommon mechanism in chronic inflammatory diseases.