Effects of Various Anti-T Cell Receptor Antibodies on the Development of Type II Collagen-Induced Arthritis in Mice

Abstract

Recent genetic studies of David and coworkers suggest that subsets of T cells utilizing specific Vβ TcR genes may play important roles in the susceptibility to collagen-induced arthritis (CIA). Hence, in vivo depletion of such T cell subsets may significantly affect the development of CIA. To address this possibility, we first examined the effects of in vivo treatments with various monoclonal antibodies (mAbs) that are specific for particular TcR Vβ families on the induction of CIA. Results presented in this study demonstrated that treatments with either anti-Vβ6, anti-Vβ8 or anti-Vβ11 did not suppress the development of arthritis in collagen-immunized mice. While combined treatments with these Vβ specific mAbs which resulted in the in vivo elimination of Vβ6⁺, Vβ8⁺ and Vβ11⁺ T cells were not very effective in preventing the onset of CIA, the severity of the arthritic disease was somewhat reduced in animals that had received the triad of anti-Vβ mAbs. By contrast, depletion of T cells expressing the αβ receptors by in vivo treatments with a pan anti-αβ mAb significantly decreased the incidence of CIA. Therefore, although an effect on the development of CIA was achieved by in vivo treatments with a mAb that detects all αβ⁺ T cells, the elimination of only a few subsets of T cells which included the Vβ6⁺, Vβ8⁺, and Vβ11⁺ cells did not profoundly alter the incidence of CIA. Finally, these results suggest that other T cell subsets expressing different TcR V genes may also contribute to the disease process of CIA.