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Clinical and Developmental Immunology
Volume 2013 (2013), Article ID 413465, 15 pages
http://dx.doi.org/10.1155/2013/413465
Review Article

Initial Immunopathogenesis of Multiple Sclerosis: Innate Immune Response

1Neuroimmunology and Neuro-Oncology Unit, Instituto Nacional de Neurología y Neurocirugía (INNN), Insurgentes Sur 3877, 14269 Mexico City, DF, Mexico
2Neurochemistry Unit, Instituto Nacional de Neurología y Neurocirugía (INNN), Insurgentes Sur 3877, 14269 Mexico City, DF, Mexico

Received 9 May 2013; Revised 1 July 2013; Accepted 9 August 2013

Academic Editor: Daniel Larocque

Copyright © 2013 Norma Y. Hernández-Pedro et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Multiple sclerosis (MS) is an inflammatory, demyelinating, and neurodegenerative disease of the central nervous system. The hallmark to MS is the demyelinated plaque, which consists of a well-demarcated hypocellular area characterized by the loss of myelin, the formation of astrocytic scars, and the mononuclear cell infiltrates concentrated in perivascular spaces composed of T cells, B lymphocytes, plasma cells, and macrophages. Activation of resident cells initiates an inflammatory cascade, leading to tissue destruction, demyelination, and neurological deficit. The immunological phenomena that lead to the activation of autoreactive T cells to myelin sheath components are the result of multiple and complex interactions between environment and genetic background conferring individual susceptibility. Within the CNS, an increase of TLR expression during MS is observed, even in the absence of any apparent microbial involvement. In the present review, we focus on the role of the innate immune system, the first line of defense of the organism, as promoter and mediator of cross reactions that generate molecular mimicry triggering the inflammatory response through an adaptive cytotoxic response in MS.