The role of IL-17A in central nervous system autoimmunity

Abstract

Multiple sclerosis (MS) is a chronic demyelinating inflammatory disorder of the central nervous system (CNS), involving autoreactive T cell responses to myelin antigens. Experimental autoimmune encephalomyelitis (EAE) is an animal model of CNS autoimmunity driven by encephalitogenic, myelin-specific Th1 and Th17 cells. Preclinical studies on the cellular and molecular mechanisms of disease in EAE increases our knowledge of the underlying basis of disease in MS patients, and assists in the discovery of novel drug targets. IL-17A and IL-17A-producing Th17 cells and γδ T cells have emerged as central players in the pathogenesis of many autoimmune diseases. Targeting the inflammatory IL-23/IL-17A immune axis has been remarkably effective in the treatment of psoriasis, and promising initial results have been reported with anti-IL-17A in MS. This study investigated the role of IL-17A in CNS inflammation using the EAE model.