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Positive or negative involvement of heat shock proteins in multiple sclerosis pathogenesis: an overview
Giuseppina Turturici1, Rosaria Tinnirello, Gabriella Sconzo
1From the Dipartimento di Scienze e Tecnologie Biologiche Chimiche e Farmaceutiche (STEBICEF) Sez Biologia Cellulare ed 16 (GT, RT, GS, FG); and Dipartimento di Biomedicina Sperimentale e Neuroscienze Cliniche (BIONEC) (GS, PR), Palermo, Italy; Department of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine, Atlanta, Georgia (AA); and Euro-Mediterranean Institute of Science and Technology, Palermo, Italy (AA, FG).
Abstract:
Multiple sclerosis (MS) is the most diffuse chronic inflammatory disease of the central nervous system. Both immune-mediated and neurodegenerative processes apparently play roles in the pathogenesis of this disease. Heat shock proteins (HSPs) are a family of highly evolutionarily conserved proteins; their expression in the nervous system is induced in a variety of pathologic states, including cerebral ischemia, neurodegenerative diseases, epilepsy, and trauma. To date, investigators have observed protective effects of HSPs in a variety of brain disease models (e.g. of Alzheimer disease and Parkinson disease). In contrast, unequivocal data have been obtained for their roles in MS that depend on the HSP family and particularly on their localization (i.e. intracellular or extracellular). This article reviews our current understanding of the involvement of the principal HSP families in MS.
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