Failure to induce experimental allergic encephalitis in mice lucking expression of SLC chemokine.

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Experimental allergic encephalitis (EAE) is a mouse model of human multiplesclerosis. Paucity of lymph node T cells (plt) mouse lacks expression of SLC (CCL21) and ELC (CCL19) chemokines. Immunization with MOG peptide induces experimental allergic encephalitis in control mice, but not in plt mice. When T cells were transferred from +/plt-C56BL/6mice immunized with MOG peptide into pltmice, EAE was deloped, suggesting that failure to develop EAE in pltmice was not due to migration failure induced by lacking chemokine expression, but due to effector T cell developmentpltmice lack expression of SLC and ELC chemokines, but T cell response to subcutaneous immunization with a protein antigen was rather higher than in control mice and prolonged much longer than in control mice. These findings suggest that T cell immune regulation is insufficient in pltmice. Apoptosis in draining lymph mode in pltmice was much less evident in pltmice than in control mice, which resulted in keeping increased number of responding T cells. To elucidate the mechanisms for the failure to develop EAE in pltmice, we will analyze effector CD4+ T cells after immunization with protein antigen