It is commonly thought that autoreactive T-cells fulfill a central role in the chronic inflammatory response that occurs in the joints of patients with rheumatoid arthritis (RA). However, the accumulated T-cells in the joints of patients with RA are functionally suppressed compared with peripheral blood T-cells. The mechanism that underlies this synovial T-cell hyporesponsiveness and the possible role of this phenomenon in the pathogenesis of RA is the subject of this article.