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The Journal of Immunology, 2001, 166: 4209-4215.
Copyright © 2001 by The American Association of Immunologists

Regulation of Experimental Autoimmune Encephalomyelitis in the C57BL/6J Mouse by NK1.1+, DX5+, {alpha}{beta}+ T Cells1

Robert B. Fritz2 and Ming-Lang Zhao

Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, WI 53226

C57BL/6 (B6) mice with targeted mutations of immune function genes were used to investigate the mechanism of recovery from experimental autoimmune encephalomyelitis (EAE). The acute phase of passive EAE in the B6 mouse is normally resolved by partial recovery followed by mild sporadic relapses. B6 TCR {beta}-chain knockout (KO) recipients of a myelin oligodendrocyte glycoprotein p35–55 encephalitogenic T cell line failed to recover from the acute phase of passive EAE. In comparison with wild-type mice, active disease was more severe in {beta}2-microglobulin KO mice. Reconstitution of TCR {beta}-chain KO mice with wild-type spleen cells halted progression of disease and favored recovery. Spleen cells from T cell-deficient mice, IL-7R KO mice, or IFN-{gamma} KO mice were ineffective in this regard. Irradiation or treatment of wild-type spleen cell population with anti-NK1.1 mAb before transfer abrogated the protective effect. Removal of DX5+ cells from wild-type spleen cells by anti-DX5 Ab-coated magnetic beads before reconstitution abrogated the suppressive properties of the spleen cells. TCR-deficient recipients of the enriched DX5+ cell population recovered normally from passively induced acute disease. DX5+ cells were sorted by FACS into DX5+ {alpha}{beta}TCR+ and DX5+ {alpha}{beta}TCR- populations. Only recipients of the former recovered normally from clinical disease. These results indicate that recovery from acute EAE is an active process that requires NK1.1+, DX5+ {alpha}{beta}+ TCR spleen cells and IFN-{gamma}.




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