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Trends Immunol. 2017 Jul;38(7):498-512. doi: 10.1016/j.it.2017.04.006. Epub 2017 May 23.

The Enigmatic Role of Viruses in Multiple Sclerosis: Molecular Mimicry or Disturbed Immune Surveillance?

Author information

1
INGM, Istituto Nazionale Genetica Molecolare 'Romeo ed Enrica Invernizzi', Milan, Italy. Electronic address: geginat@ingm.org.
2
INGM, Istituto Nazionale Genetica Molecolare 'Romeo ed Enrica Invernizzi', Milan, Italy.
3
INGM, Istituto Nazionale Genetica Molecolare 'Romeo ed Enrica Invernizzi', Milan, Italy; Department of Medical Biotechnology and Translational Medicine, University of Milan, Milan, Italy.
4
Department of Pathophysiology and Transplantation, University of Milan, Centro Dino Ferrari, Milan, Italy; Fondazione Cá Granda, IRCCS Ospedale Policlinico, Milan, Italy.
5
INGM, Istituto Nazionale Genetica Molecolare 'Romeo ed Enrica Invernizzi', Milan, Italy; DISCCO, Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy.

Abstract

Multiple sclerosis (MS) is a T cell driven autoimmune disease of the central nervous system (CNS). Despite its association with Epstein-Barr Virus (EBV), how viral infections promote MS remains unclear. However, there is increasing evidence that the CNS is continuously surveyed by virus-specific T cells, which protect against reactivating neurotropic viruses. Here, we discuss how viral infections could lead to the breakdown of self-tolerance in genetically predisposed individuals, and how the reactivations of viruses in the CNS could induce the recruitment of both autoaggressive and virus-specific T cell subsets, causing relapses and progressive disability. A disturbed immune surveillance in MS would explain several experimental findings, and has important implications for prognosis and therapy.

PMID:
28549714
DOI:
10.1016/j.it.2017.04.006
[Indexed for MEDLINE]

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