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

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An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	The Enigmatic Role of Viruses in Multiple Sclerosis: Molecular Mimicry or Disturbed Immune Surveillance?
Creator	Abrignani, Sergio De Francesco, Raffaele Galimberti, Daniela Geginat, Jens Pagani, Massimiliano Paroni, Moira Scarpini, Elio T D $ D I F F ], _
Source	Elsevier; Medline; PMC
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.
has issue date	2017-07-31(xsd:dateTime)
bibo:doi	10.1016/j.it.2017.04.006
bibo:pmid	28549714
has license	els-covid
sha1sum (hex)	4eecd2d9c023f1c31011a08941d4b07a868d930e
schema:url	https://doi.org/10.1016/j.it.2017.04.006
resource representing a document's title	The Enigmatic Role of Viruses in Multiple Sclerosis: Molecular Mimicry or Disturbed Immune Surveillance?
has PubMed Central identifier	PMC7185415
has PubMed identifier	28549714
schema:publication	Trends in Immunology
resource representing a document's body	covid:4eecd2d9c023f1c31011a08941d4b07a868d930e#body_text
is schema:about of	named entity 'MULTIPLE SCLEROSIS' named entity 'IMMUNE SURVEILLANCE' named entity 'CENTRAL NERVOUS SYSTEM' named entity 'RECRUITMENT' named entity 'AUTOIMMUNE DISEASE' named entity 'SPECIFIC' named entity 'VIRAL INFECTIONS' named entity 'PROMOTE' named entity 'A T' named entity 'PROGNOSIS' named entity 'IMPORTANT' named entity 'UNCLEAR' named entity 'BREAKDOWN' named entity 'FINDINGS' named entity 'T CELL' named entity 'EPSTEIN-BARR VIRUS' covid:arg/4eecd2d9c023f1c31011a08941d4b07a868d930e named entity 'ASSOCIATION' named entity 'PREDISPOSED' named entity 'HERE' named entity 'NEUROTROPIC' named entity 'PROGRESSIVE' named entity 'IS A' named entity 'ITS' named entity 'T CELL SUBSETS' named entity 'EXPERIMENTAL' named entity 'DRIVEN' named entity 'DISABILITY' named entity 'RELAPSES' named entity 'CNS' named entity 'SELF-TOLERANCE' named entity 'VIRUSES' named entity 'ROLE' named entity 'DISCUSS' named entity 'EVIDENCE' named entity 'VIRUS' named entity 'THERAPY' named entity 'MOLECULAR MIMICRY' named entity 'T CELLS' named entity 'INCREASING' named entity 'INDUCE' named entity 'MULTIPLE SCLEROSIS' named entity 'INDIVIDUALS' named entity 'LEAD' named entity 'IMMUNE SURVEILLANCE' named entity 'VIRUSES' named entity 'CAUSING' named entity 'HOW' named entity 'viruses' named entity 'genetically predisposed' named entity 'CNS' named entity 'Epstein-Barr Virus' named entity 'viruses' named entity 'autoimmune disease' named entity 'Molecular Mimicry' named entity 'Immune Surveillance' named entity 'CD4 +' named entity 'cell clones' named entity 'antigens' named entity 'virus' named entity 'thymus' named entity 'viral infections' named entity 'Th17' named entity 'effector T cells' named entity 'CXCR3' named entity 'GM-CSF' named entity 'PML' named entity 'Epstein-Barr virus' named entity 'high-risk' named entity 'PML' named entity 'IFN-g' named entity 'allele' named entity 'allogenic' named entity 'Th1'

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