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The exact mechanism of glatiramer acetate (GA, Copaxone®), an FDA-approved immunomodulatory therapy for multiple sclerosis (MS), remains unclear after decades of research. Previously, we have shown that GA therapy of MS induces CD8 +  T cell responses that can potentially suppress pathogenic CD4 +  T cell responses. Using a murine model of MS, experimental autoimmune encephalomyelitis (EAE), we now demonstrate that CD8 +  T cells are necessary in mediating the therapeutic effects of GA. Further, adoptive transfer of GA-induced CD8 +  T cells resulted in amelioration of EAE, establishing a role as a viable immunotherapy in demyelinating disease. Generation of these cells required indoleamine-2,3-dioxygenase (IDO), while suppressive function depended on non-classical MHC class I, IFN-γ, and perforin expression. GA-induced regulatory myeloid cells, previously shown to activate CD4 +  regulatory T cells in an antigen-independent manner, required CD8 +  T cells for disease suppression  in vivo . These studies demonstrate an essential role for CD8 +  T cells in GA therapy and identify their potential as an adoptive immunotherapeutic agent.

CD8+ T Cells Are Required For Glatiramer Acetate Therapy in Autoimmune Demyelinating Disease