T cell mediated pathogenesis in EAE: Molecular mechanisms

Biomed J. May-Jun 2015;38(3):183-93. doi: 10.4103/2319-4170.155590.

Abstract

T cells are major initiators and mediators of disease in multiple sclerosis (MS) and in its animal model experimental autoimmune encephalomyelitis (EAE). EAE is an antigen-driven autoimmune model in which immunization against myelin autoantigens elicits strong T cell responses which initiate its pathology with CNS myelin destruction. T cells cause pathogenic events by several mechanisms; some work in a direct fashion in the CNS, such as direct cytokine-induced damage, granzyme-mediated killing, or glutamate-induced neurotoxicity, whereas most are indirect mechanisms, such as activation of other cell types like macrophages, B cells, or neutrophils. This review aims to describe and discuss the molecular effector mechanism by which T cells harm the CNS during EAE.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • B-Lymphocytes / immunology*
  • Central Nervous System / immunology*
  • Cytokines / immunology
  • Cytokines / metabolism
  • Encephalomyelitis, Autoimmune, Experimental / immunology*
  • Humans
  • Multiple Sclerosis / immunology*
  • T-Lymphocytes / immunology*

Substances

  • Cytokines