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

T cell mediated pathogenesis in EAE: Molecular mechanisms.

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Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.


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.

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