Experimental allergic encephalomyelitis in susceptible and resistant strains of mice after adoptive transfer of T cells activated by antibodies to the T cell receptor complex

Lymphoid cells from normal and myelin basic protein (MBP)-immune PL/J, SJL/J and ( SJL × PL)F1 hybrid mice were activated by in vitro culture with monoclonal antibodies specific for CD3 or specific T cell receptor (TCR) V β chains. Lymphoid cells activated in this manner from MBP-immune animals did not readily transfer experimental acute encephalomyelitis (EAE) to naive syngeneic recipients in contrast to lymphoid cells from the same source cultured with concanavalin A (ConA) or myelin basic protein (MBP). However, recipients of anti-TCR antibody-activated MBP-specific blasts showed accelerated onset and increased severity of EAE following immunization with MBP as compared to unmanipulated control animals. Anti-TCR activated cells incorporated [ 3H]-thymidine at a level comparable to ConA or antigen-stimulated cells and secreted interleukin (IL)-2 at comparable levels Anti-TCR activated blasts were > 90% positive for CD3 and α/βTCR, 60% CD4 + and 30% CD8 +. PL/J or (SJL × PL)F1 recipients of anti-TCR-activated spleen cells from syngeneic normal mice also had more EAE than control mice following immunization with MBP. Non-responder C57BL/10SnJ mice could be converted to responders by infusion of anti-CD3 or anti-V β8 monoclonal antibody-treated syngeneic spleen cells taken from normal syngeneic unimmunized mice.