The contribution of T cells to the pathogenesis of rheumatoid arthritis (RA) has been a matter of debate which is addressed in a number of reviews and chapters of this book [1-3]. The contribution of monocytes through the production of proinflammatory cytokines has been simpler to demonstrate [4]. Accordingly, Interleukin (IL)-l and tumor necrosis factor (TNF) a have been selected as important therapeutic targets [5].

With respect to the production of T cell derived cytokines in RA, the low level of expression and production by RA synovium of T cell derived cytokines was first described for IL-2 and Interferon (IFN) y, then extended to TNF~ and IL-4 [6-9]. The relative failure to detect these factors has been one reason to question the role of T cells. However, another way to look at the contribution of T cells in RA focuses on the analysis of their cytokine profile and the associated subsets of T cells. Indeed, such subsets have been associated with the development of different disease patterns in mouse and man. More importantly, the modulation of such cytokine profiles is now considered a therapeutic goal [10].