Evidence map›Paper›PMID 23947356›Full record

ReviewImmunological reviews2013

Virus infection, antiviral immunity, and autoimmunity.

Daniel R Getts, Emily M L Chastain, Rachael L Terry, Stephen D Miller

Open access · greenAbstract readReview
In one paragraph

Review in Immunological reviews, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 177 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
177citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% of its field
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

177 citing papers in PubMed, 1 synthesis or guideline pooled it, 296 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
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  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. HE4: a potential diagnostic biomarker in autoimmune diseases.Central-European journal of immunology · 2026
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Differential roles of human CD4Nature immunology · 2025
    Article
  20. Review

117 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Daniel R GettsDepartment of Microbiology-Immunology and Interdepartmental Immunobiology Center, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Emily M L Chastain
Rachael L Terry
Stephen D Miller
Northwestern University · US

Funding

IMMUNOREGULATION AND PATHOLOGY OF CHRONIC-RELAPSING EAER01NS026543 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MILLER, STEPHEN D · 1988 to 2016
$5.0M
A VIRUS-INDUCED MOLECULAR MIMICRY MODEL OF MSR01NS040460 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MILLER, STEPHEN D · 2000 to 2008
$2.6M
Innate Regulation and CD4+Th1/17 Immunity in TMEV-Induced DemyelinationR01NS062365 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MILLER, STEPHEN D · 2010 to 2014
$1.6M
NINDS NIH HHS R01 NS026543NINDS NIH HHS R01 NS040460NINDS NIH HHS R01 NS062365
6 · The paper itself

Abstract

As a group of disorders, autoimmunity ranks as the third most prevalent cause of morbidity and mortality in the Western World. However, the etiology of most autoimmune diseases remains unknown. Although genetic linkage studies support a critical underlying role for genetics, the geographic distribution of these disorders as well as the low concordance rates in monozygotic twins suggest that a combination of other factors including environmental ones are involved. Virus infection is a primary factor that has been implicated in the initiation of autoimmune disease. Infection triggers a robust and usually well-coordinated immune response that is critical for viral clearance. However, in some instances, immune regulatory mechanisms may falter, culminating in the breakdown of self-tolerance, resulting in immune-mediated attack directed against both viral and self-antigens. Traditionally, cross-reactive T-cell recognition, known as molecular mimicry, as well as bystander T-cell activation, culminating in epitope spreading, have been the predominant mechanisms elucidated through which infection may culminate in an T-cell-mediated autoimmune response. However, other hypotheses including virus-induced decoy of the immune system also warrant discussion in regard to their potential for triggering autoimmunity. In this review, we discuss the mechanisms by which virus infection and antiviral immunity contribute to the development of autoimmunity.

Indexed as

AutoimmunityAnimalsAutoimmune DiseasesCentral Nervous SystemHumansVirus DiseasesVirusesautoimmune diseasebystander activationepitope spreadingmicrobial superantigensmolecular mimicryT-cell receptor affinity

Identifiers

PMID23947356
PMCPMC3971377
OpenAlexW2075653203

What OpenQuestion holds

Textmetadata
LicenceTDM
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.