Late Complications of Immune Deviation Therapy in a Nonhuman Primate

作者：Claude P. Genain, Kristina Abel, Nicole A. Belmar, Francois J. Villinger, Daniel P. Rosenberg, Christopher Linington, Cedric S. Raine, Stephen L. Hauser · 发表于：Science · 年份：1996 · DOI：10.1126/science.274.5295.2054 · 被引用次数：322 · 研究领域：T-cell and B-cell Immunology、Immunotherapy and Immune Responses、Multiple Sclerosis Research Studies

The administration of antigens in soluble form can induce antigen-specific immune tolerance and suppress experimental autoimmune diseases. In a marmoset model of multiple sclerosis induced by myelin oligodendrocyte glycoprotein (MOG), marmosets tolerized to MOG were protected against acute disease, but after tolerization treatment a lethal demyelinating disorder emerged. In these animals, MOG-specific T cell proliferative responses were transiently suppressed, cytokine production was shifted from a T helper type 1 (TH1) to a TH2 pattern, and titers of autoantibodies to MOG were enhanced. Thus, immune deviation can increase concentrations of pathogenic autoantibodies and in some circumstances exacerbate autoimmune disease.