NEUROINFLAMMATORY MECHANISMS OF CYTOKINES IN MULTIPLE SCLEROSIS

Abstract

Multiple Sclerosis (MS) is an autoimmune disease characterized by the inflammatory demyelination of neurons in the central nervous system (CNS). There are various cytokines involves in the pathogenesis of Multiple Sclerosis such as interferon-γ (INF-γ), tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1β), osteopontin, interleukin-3 (IL3), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-10 (IL-10), interleukin-12 (IL-12), interleukin-18 (IL-108) and transforming growth factor-β (TGF- β). Mostly used animal models for Multiple Sclerosis is experimental autoimmune encephalomyelitis (EAE). A model induced in Dark Agouti rats by immunization with the N-terminal fragment of myelin oligodendrocyte glycoprotein. Moreover, CD4+ or T helper cells also play an important role in the initiation of antigen-specific immune responses. It is possible to regulate the immune response and induce tolerance to disease through manipulation of the T helper response. In the present study a detailed review on role of cytokines in Multiple Sclerosis shell carried out.