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T Cell Regulation of IFN- Production by Central Nervous System-Infiltrating Encephalitogenic T Cells: Correlation with Recovery from Experimental Autoimmune Encephalomyelitis¹

Eugene D. Ponomarev^*, Marina Novikova^*, Maryam Yassai^*, Marian Szczepanik, Jack Gorski^* and Bonnie N. Dittel^2,*

^* Blood Research Institute, Blood Center of Southeastern Wisconsin, Milwaukee, WI 53201; and Department of Human Developmental Biology, College of Medicine, Jagiellonian University, Kraków, Poland

Interferon- has been shown to be important for the resolution of inflammation associated with CNS autoimmunity. Because one of the roles of T cells is the regulation of inflammation, we asked whether T cells were able to regulate CNS inflammation using the autoimmune disease mouse model experimental autoimmune encephalomyelitis (EAE). We show that the presence of T cells was needed to promote the production of IFN- by both CD4 and CD8 T cells in the CNS before the onset of EAE. This regulation was shown to be independent of the ability of T cells to produce IFN-, and was specific to T cells in the CNS, as no alterations in IFN- production were detectable in T cell-deficient mice in the spleen and lymph nodes of mice with EAE or following immunization. Analysis of TCR gene usage in the CNS showed that the only TCR V gene families present in the CNS before EAE onset are from the DV7s6 and DV105s1 gene families. We also show that the primary IFN--producing cells in the CNS are the encephalitogenic T cells, and that T cell-deficient mice are unable to resolve EAE disease symptoms like control mice, thus exhibiting a long-term chronic disease course similar to that observed in IFN--deficient mice. These data suggest that CNS resident T cells promote the production of IFN- by encephalitogenic T cells in the CNS, which is ultimately required for the recovery from EAE.

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