Mechanisms regulating regional localization of inflammation during CNS autoimmunity

Authors


Joan Goverman
Department of Immunology, University of Washington
Office H564, HSC, Box 357650, 1959 NE Pacific Street
Seattle, WA 98195, USA
Tel.: +1 206 685 7604
Fax: +1 206 543 1013
e-mail: goverman@uw.edu

Abstract

Summary:  Multiple sclerosis (MS) is a disease of the central nervous system (CNS) characterized by inflammatory, demyelinating lesions localized in the brain and spinal cord. Experimental autoimmune encephalomyelitis (EAE) is an animal model of MS that is induced by activating myelin-specific T cells and exhibits immune cell infiltrates in the CNS similar to those seen in MS. Both MS and EAE exhibit disease heterogeneity, reflecting variations in clinical course and localization of lesions within the CNS. Collectively, the differences seen in MS and EAE suggest that the brain and spinal cord function as unique microenvironments that respond differently to infiltrating immune cells. This review addresses the roles of the cytokines interferon-γ and interleukin-17 in determining the localization of inflammation to the brain or spinal cord in EAE.

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