Abstract

The question of whether a cell-mediated or a humoral mechanism initiates EAE in rats sensitized with BP-CFA was investigated. The requirement of T cells for EAE induction was manifested when Tx, irradiated rats were reconstituted with normal lymphoid cells treated with ATS and then injected with BP-CFA. Neither EAE nor antibody was produced, indicating the T cell dependency of BP specific antibody production. More precise information regarding the role of the T cell in the production of EAE was obtained by means of passive transfer of EAE with sensitized lymphocytes. Thus, transfer of lymphoid cells from rats previously sensitized to BP-CFA into Tx, irradiated rats elicited EAE and antibodies to BP. However, no EAE followed when the transferred cells were first depleted of T cells by treatment with ATS. Nevertheless, ATP pretreatment did not depress the levels of antibody to BP produced in the transfer recipients. The latter finding indicates that the cells from animals sensitized 9 days previously were already committed to the production of antibodies to BP. Therefore, a) T cells are absolutely necessary for induction of EAE and b) antibody detected by antigen-binding is not responsible for the pathogenesis of this disease.

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