Vaccination against experimental autoimmune encephalomyelitis using a subencephalitogenic dose of autoimmune effector T cells. (2). Induction of a protective anti-idiotypic response.

We previously reported that a subencephalitogenic dose (10(4) of activated anti-BP Z1a T cells rendered Lewis rats significantly resistant to EAE induced either actively or adoptively. This resistance was specific to EAE and persisted for over 4 months. The experiments reported in this paper were done to investigate the mechanisms of this resistance. We found that the state of vaccination was marked by a decrease in the in vitro proliferation and in vivo DTH responses to BP. Resistance could be transferred to recipient rats with the thymus or spleen cells of donor vaccinated rats. Vaccination led to the appearance of proliferative and DTH responses that were specifically directed to the Z1a T cells. The kinetics and compartmentalization of this anti-idiotypic responsiveness was studied by vaccinating rats in the hind footpads and monitoring the proliferative reactivity of the draining popliteal lymph node (PLN) and distal cervical lymph node (CLN) cells at various times. We found that the anti-idiotypic reactivity was confined to the PLN on days 5-6 and thereafter became systemic. Excision of the PLN on day 6, but not on days 3 or 11, robbed the rats of their acquired resistance to EAE. In contrast, the PLN cells of the vaccinated rats transferred resistance to naive donors. Thus, the lymphoid population containing cell-mediated anti-idiotypic responsiveness served as a vehicle of resistance. These results suggest that anti-idiotypic T-cell immunity to autoimmune effector T cells is involved in the resistance to EAE induced by T-cell vaccination.