DELAYED-TYPE HYPERSENSITIVITY RESPONSE IN EXPERIMENTAL AUTOIMMUNE NEURITIS TREATED WITH PEPTIDE-COUPLED SPLEEN-CELLS

Experimental autoimmune neuritis (EAN) is a T cell-mediated autoimmune inflammatory disease of the peripheral nervous system that is characterized by demyelination and mononuclear cell infiltration. It is induced in Lewis rats by administration of myelin P-2 protein or a synthetic peptide (SP-26) corresponding to amino acid residues 53-78 of bovine P-2 protein. Recently, we showed that SP-26, when coupled to syngeneic spleen cells and administered intravenously, provided an effective means of inducing tolerance by inhibiting the clinical signs, decreased proliferative response of lymphoid cells to SP-26 and histological changes of EAN. However, our current data indicate that, despite tolerance induction in these Lewis rats, the antigen-specific delayed-type hypersensitivity (DTH) response to SP-26 remained intact. Furthermore, interferon (IFN)-gamma production by spleen cells of tolerized rats were unchanged as compared to EAN rats. The in vitro proliferation of T lymphocytes from tolerized rats stimulated by SP-26 was reduced as compared to EAN controls but was enhanced upon addition of exogenous interleukin-2 Thus, reduction in EAN clinical signs does not necessarily indicate a decrease in DTH response and IFN-gamma production in EAN Lewis rats. The implication of this finding in regard to immunoregulatory mechanism of DTH response is discussed.