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Chemokines and Transcription Factors in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis
Cai Yingying, Du Changsheng*
Laboratory of Receptor-based Bio-medicine, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China
Abstract: Multiple sclerosis (MS) is a demyelinating inflammatory disorder of the central nervous system. The experimental autoimmune encephalomyelitis (EAE) shares clinical and pathological features with MS and is widely used as the animal model for MS. The Pathogenesis of MS is still unknown, but it is widely accepted that MS is a CD4+ T cell-mediated autoimmune disease of the central nervous system which is based on susceptibility genes and triggered by environmental factors. Upon T-cell receptor (TCR)-mediated cell activation, naive CD4+ T cells can differentiate into at least four major lineages, TH1, TH2, TH17 and iTreg cells, which participate in different types of immune responses. Networks of cytokines and transcription factors are critical for CD4+ T cell differentiation and effector cytokine production. This article will review the collaboration and cross-regulation between various essential cytokines and transcription factors during the process of CD4+ T cell differentiation towards distinct lineages, as well as in the process of MS/EAE. Understanding the roles of key cytokines and transcription factors in these processes will help to understand disease pathogenesis and supply indications for disease therapy.