PREVENTION AND TREATMENT OF LEWIS RAT EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS WITH A MONOCLONAL-ANTIBODY TO THE T-CELL RECEPTOR V-BETA-8.2 SEGMENT

The predominance of T cell receptor (TCR) V beta 8.2 utilization by en cephalitogenic T cells induced in Lewis rats by immunization with myel in basic protein (MBP) is controversial. Thus, both an almost exclusiv e usage of V beta 8.2 [Burns, ER., Li, X., Shen, N., Offner, H., Chou, Y. K., Vandenbark, A. A. and Heber-Katz, E., J. Exp. Med. 1989. 169: 27; Chluba, J., Steeg, C., Becker, A., Wekerle, H. and Epplen, J. T., fur. J. Immunol. 1989. 19: 279] and a quite diverse V beta composition of CD4 T cells causing experimental autoimmune encephalomyelitis (EAE ) [Sun, D., Gold, P. D., Smith, L., Brostoff, S. and Cole dough, C., E ur. J. Immunol. 1992. 22: 591; Sun, D., Le, J. and Coleclough, C., Eur . J. Immunol. 1993. 23: 494] have been reported. Using a recently deve loped monoclonal antibody (mAb) specific for TCR V beta 8.2, we show t hat postnatal treatment effectively eliminates V beta 8.2-bearing cell s and prevents MBP-induced EAE in the majority of Lewis rats. Moreover , treatment of adult Lewis rats with V beta 8.2-specific mAb as late a s on day 12 after MBP immunization suppressed the development of neuro logical symptoms. Thus, V beta 8.2-bearing cells do play a decisive ro le in Lewis rat EAE, and suppression of the small (5%) V beta 8.2-expr essing T cell subset provides an effective therapeutic strategy.