Diverse T cell receptor beta chain usage by rat encephalitogenic T cells reactive to residues 68-88 of myelin basic protein.

Encephalitogenic T cells not only cause experimental autoimmune encephalomyelitis (EAE), but they induce resistance against subsequent induction of the disease as well. The T cell receptor (TcR) of encephalitogenic T cells is believed to contribute to their vaccinating activity. Findings in support of this assumption include the apparent restricted use of particular TcR elements, such as V beta 8.2. However, results from other laboratories including ours do not support this idea. We previously showed that rat T cells reactive against the conserved encephalitogenic epitope of myelin basic protein [MBP (87-99)] use the TcR in a heterogeneous fashion (Sun, D. et al., Eur. J. Immunol. 1992. 22: 591). Here we show, in Lewis rats, that the TcR beta chain usage of T cells specific for the dominant MBP (68-88) epitope is not restricted to V beta 8.2. Not only did such cells rely on diverse V beta chains, but some non-V beta 8-bearing cells were highly encephalitogenic. We also show that antigen-presenting cells (APC) play an important role in determining the TcR usage of MBP-specific T cells. Stimulation of MBP (68-88)-specific T cell lines by cloned APC derived from different sources resulted in selection of encephalitogenic T cells bearing different TcR beta chains.