Evidence map›Paper›PMID 12050361›Full record

ArticleJournal of virology2002

Gammadelta T cells promote a Th1 response during coxsackievirus B3 infection in vivo: role of Fas and Fas ligand.

Sally Huber, Cuixia Shi, Ralph C Budd

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. A viral-specific CD4Frontiers in immunology · 2023
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Role of gamma-delta T cells in liver inflammation and fibrosis.World journal of gastrointestinal pathophysiology · 2014
    Review
  10. Article
  11. Article
  12. Article
  13. TLR3 deficiency induces chronic inflammatory cardiomyopathy in resistant mice following coxsackievirus B3 infection: role for IL-4.American journal of physiology. Regulatory, integrative and comparative physiology · 2013
    Article
  14. Article
  15. Pathogenesis and diagnosis of myocarditis.Heart (British Cardiac Society) · 2012
    Review
  16. Article
  17. Article
  18. Review
  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

3 authors at 1 institution in 1 country.

Sally HuberDepartment of Pathology, College of Medicine, The University of Vermont, Burlington, VT 05405, USA. Sally.Huber@uvm.edu
Cuixia Shi
Ralph C Budd
University of Vermont · US

Funding

Synovial V delta 1 cells kill Th2 cellsP01AI045666 · NIAID · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI BUDD, RALPH C · 1999 to 2010
$12.5M
TH1 AND TH2 RESPONSES IN PATHOGENIC CVB3 INFECTIONSR01HL058583 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI HUBER, SALLY A. · 1998 to 2005
$871k
NHLBI NIH HHS HL 58583NHLBI NIH HHS R01 HL058583NIAID NIH HHS AI 45666NIAID NIH HHS P01 AI045666
6 · The paper itself

Abstract

Fas/Fas ligand (FasL) interactions regulate disease outcome in coxsackievirus B3 (CVB3)-induced myocarditis. MRL(+/+) mice infected with CVB3 develop severe myocarditis, a dominant CD4(+) Th1 (gamma interferon [IFN-gamma(+)]) response to the virus, and a predominance of gammadelta T cells in the myocardial infiltrates. MRL lpr/lpr and MRL gld/gld mice, which lack normal expression of Fas and express a mutated FasL, respectively, have minimal myocarditis and show a dominant CD4(+) Th2 (interleukin-4 [IL-4(+)]) phenotype to CVB3. Spleen cells from virus-infected wild-type, lpr, and gld animals proliferate equally to virus in vitro. Adoptive transfer of gammadelta T cells from hearts of CVB3-infected MRL(+/+) mice (FasL(+)) into infected MRL gld/gld recipients (FasL(-)/Fas(+)) restores both disease susceptibility and Th1 cell phenotype. However, transfer of these cells into MRL lpr/lpr recipients (FasL(+)/Fas(-)) did not promote myocarditis and the viral response remained Th2 biased. This paralleled the expression of very high surface levels of FasL by myocardial gammadelta T cells, as well as their propensity to selectively lyse Th2 virus-specific CD4(+) T cells. These results demonstrate that Fas/FasL interactions conferred by gammadelta T cells on lymphocyte subpopulations may regulate the cytokine response to CVB3 infection and pathogenicity.

Indexed as

AnimalsEnterovirus B, HumanEnterovirus InfectionsFas Ligand Proteinfas ReceptorInterferon-gammaMembrane GlycoproteinsMiceMice, Inbred BALB CMice, Inbred MRL lprMyocarditisReceptors, Antigen, T-Cell, gamma-deltaTh1 CellsFASLG protein, humanFas Ligand ProteinFasl protein, mousefas ReceptorInterferon-gammaMembrane GlycoproteinsReceptors, Antigen, T-Cell, gamma-delta

Identifiers

PMID12050361
PMCPMC136276
OpenAlexW2121005745

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.