Evidence map›Paper›PMID 28549714›Full record

ReviewTrends in immunology2017

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

Jens Geginat, Moira Paroni, Massimiliano Pagani, Daniela Galimberti, Raffaele De Francesco, Elio Scarpini, Sergio Abrignani

Abstract readReview
In one paragraph

Review in Trends in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

39 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Inflammasome Molecular Insights in Autoimmune Diseases.Current issues in molecular biology · 2024
    Review
  6. Article
  7. Review
  8. Antibody Cross-Reactivity in Auto-Immune Diseases.International journal of molecular sciences · 2023
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. The Role of Exposomes in the Pathophysiology of Autoimmune Diseases II: Pathogens.Pathophysiology : the official journal of the International Society for Pathophysiology · 2022
    Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Jens GeginatINGM, Istituto Nazionale Genetica Molecolare 'Romeo ed Enrica Invernizzi', Milan, Italy. Electronic address: geginat@ingm.org.
Moira ParoniINGM, Istituto Nazionale Genetica Molecolare 'Romeo ed Enrica Invernizzi', Milan, Italy.
Massimiliano PaganiINGM, Istituto Nazionale Genetica Molecolare 'Romeo ed Enrica Invernizzi', Milan, Italy; Department of Medical Biotechnology and Translational Medicine, University of Milan, Milan, Italy.
Daniela GalimbertiDepartment of Pathophysiology and Transplantation, University of Milan, Centro Dino Ferrari, Milan, Italy; Fondazione Cá Granda, IRCCS Ospedale Policlinico, Milan, Italy.
Raffaele De FrancescoINGM, Istituto Nazionale Genetica Molecolare 'Romeo ed Enrica Invernizzi', Milan, Italy.
Elio ScarpiniDepartment of Pathophysiology and Transplantation, University of Milan, Centro Dino Ferrari, Milan, Italy; Fondazione Cá Granda, IRCCS Ospedale Policlinico, Milan, Italy.
Sergio AbrignaniINGM, Istituto Nazionale Genetica Molecolare 'Romeo ed Enrica Invernizzi', Milan, Italy; DISCCO, Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Immunologic SurveillanceCell MovementCentral Nervous SystemCytokinesEpstein-Barr Virus InfectionsGene-Environment InteractionGene Expression RegulationGenetic Predisposition to DiseaseHerpesvirus 4, HumanHost-Pathogen InteractionsHumansMolecular MimicryMultiple SclerosisReceptors, CytokineTh17 CellsTh1 CellsCytokinesReceptors, Cytokine

Identifiers

PMID28549714
PMCPMC7185415

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.