EFFECTS OF VARIOUS ANTI-T CELL-RECEPTOR ANTIBODIES ON THE DEVELOPMENTOF TYPE-II COLLAGEN-INDUCED ARTHRITIS IN MICE

Recent genetic studies of David and coworkers suggest that subsets of T cells utilizing specific Vbeta TcR genes may play important roles in the susceptibility to collagen-induced arthritis (CIA). Hence, in viv o depletion of such T cell subsets may significantly affect the develo pment of CIA. To address this possibility, we first examined the effec ts of in vivo treatments with various monoclonal antibodies (mAbs) tha t are specific for particular TcR Vbeta families on the induction of C IA. Results presented in this study demonstrated that treatments with either anti-Vbeta6, anti-Vbeta8 or anti-Vbeta11 did not suppress the d evelopment of arthritis in collagen-immunized mice. While combined tre atments with these Vbeta specific mAbs which resulted in the in vivo e limination of Vbeta6+, Vbeta8+ and Vbeta11+ T cells were not very effe ctive in preventing the onset of CIA, the severity of the arthritic di sease was somewhat reduced in animals that had received the triad of a nti-Vbeta mAbs. By contrast, depletion of T cells expressing the alpha beta receptors by in vivo treatments with a pan anti-alphabeta mAb sig nificantly decreased the incidence of CIA. Therefore, although an effe ct on the development of CIA was achieved by in vivo treatments with a mAb that detects all alphabeta+ T cells, the elimination of only a fe w subsets of T cells which included the Vbeta6+, Vbeta8+, and Vbeta11 cells did not profoundly alter the incidence of CIA. Finally, these r esults suggest that other T cell subsets expressing different TcR V ge nes may also contribute to the disease process of CIA.