title: Initial immunopathogenesis of multiple sclerosis: innate immune response.
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.
authors.affiliation: Neuroimmunology and Neuro-Oncology Unit, Instituto Nacional de Neurología y Neurocirugía (INNN), Insurgentes Sur 3877, 14269 Mexico City, DF, Mexico.
authors.forename: Norma Y
authors.initials: NY
authors.lastname: Hernández-Pedro
authors.forename: Guillermo
authors.initials: G
authors.lastname: Espinosa-Ramirez
authors.forename: Verónica Pérez
authors.initials: VP
authors.lastname: de la Cruz
authors.forename: Benjamín
authors.initials: B
authors.lastname: Pineda
authors.forename: Julio
authors.initials: J
authors.lastname: Sotelo
mesh_terms: D000818:Animals; D001812:Blood-Brain Barrier / Q000276:immunology / Q000378:metabolism; D002450:Cell Communication; D004195:Disease Models, Animal; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D042783:Endothelial Cells / Q000276:immunology / Q000378:metabolism; D006360:Heat-Shock Proteins / Q000378:metabolism; D006801:Humans; D007113:Immunity, Innate; D007155:Immunologic Factors / Q000627:therapeutic use; D007249:Inflammation / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D007962:Leukocytes / Q000276:immunology / Q000378:metabolism; D009103:Multiple Sclerosis / Q000188:drug therapy / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism
chemical_list: D006360:Heat-Shock Proteins; D007155:Immunologic Factors; D018160:Receptors, Cytoplasmic and Nuclear