Evidence map›Paper›PMID 11390587›Full record

ArticleJournal of virology2001

Cytokine production by Vgamma(+)-T-cell subsets is an important factor determining CD4(+)-Th-cell phenotype and susceptibility of BALB/c mice to coxsackievirus B3-induced myocarditis.

S A Huber, D Graveline, W K Born, R L O'Brien

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

40 citing papers in PubMed, 76 citations in OpenAlex.

  1. Review
  2. Article
  3. CCR6The Journal of investigative dermatology · 2019
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  19. Regulation and function of IL-17A- and IL-22-producing γδ T cells.Cellular and molecular life sciences : CMLS · 2011
    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

4 authors at 3 institutions in 1 country.

S A HuberDepartment of Pathology, University of Vermont, Burlington, Vermont, USA. shuber@salus.med.uvm.edu
D Graveline
W K Born
R L O'Brien
University of Vermont · USNational Jewish Health · USUniversity of Colorado Denver · US

Funding

The Basis of Functional Variation in Gamma/Delta T cellsR01AI044920 · NIAID · NATIONAL JEWISH HEALTH · PI O'BRIEN, REBECCA L. · 1999 to 2009
$3.0M
RESPONSE OF GAMMA/DELTA T CELLS TO CARDIOLIPIN AND DNAR01AI040611 · NIAID · NATIONAL JEWISH HEALTH · PI BORN, WILLI K · 1997 to 2004
$1.3M
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 R01 HL058583NHLBI NIH HHS R01 HL58583NIAID NIH HHS R01 AI040611NIAID NIH HHS R01 AI044920NIAID NIH HHS R01 AI40611NIAID NIH HHS R01 AI44920
6 · The paper itself

Abstract

Two coxsackievirus B3 (CVB3) variants (H3 and H310A1) differ by a single amino acid mutation in the VP2 capsid protein. H3 induces severe myocarditis in BALB/c mice, but H310A1 is amyocarditic. Infection with H3, but not H310A1, preferentially activates Vgamma4 Vdelta4 cells, which are strongly positive for gamma interferon (IFN-gamma), whereas Vgamma1 Vdelta4 cells are increased in both H3 and H310A1 virus-infected animals. Depletion of Vgamma1(+) cells using monoclonal anti-Vgamma1 antibody enhanced myocarditis and CD4(+)-, IFN-gamma(+)-cell responses in both H3- and H310A1-infected mice yet decreased the CD4(+)-, IL-4(+)-cell response. Depleting Vgamma4(+) cells suppressed myocarditis and reduced CD4(+) IFN-gamma(+) cells but increased CD4(+) IL-4(+) T cells. The role of cytokine production by Vgamma1(+) and Vgamma4(+) T cells was investigated by adoptively transferring these cells isolated from H3-infected BALB/c Stat4 knockout (Stat4ko) (defective in IFN-gamma expression) or BALB/c Stat6ko (defective in IL-4 expression) mice into H3 virus-infected wild-type BALB/c recipients. Vgamma4 and Vgamma1(+) T cells from Stat4ko mice expressed IL-4 but no or minimal IFN-gamma, whereas these cell populations derived from Stat6ko mice expressed IFN-gamma but no IL-4. Stat4ko Vgamma1(+) cells (IL-4(+)) suppress myocarditis. Stat6ko Vgamma1(+) cells (IFN-gamma(+)) were not inhibitory. Stat6ko Vgamma4(+) cells (IFN-gamma(+)) significantly enhanced myocarditis. Stat4ko Vgamma4(+) cells (IL-4(+)) neither inhibited nor enhanced disease. These results show that distinct gammadelta-T-cell subsets control myocarditis susceptibility and bias the CD4(+)-Th-cell response. The cytokines produced by the Vgamma subpopulation have a significant influence on the CD4(+)-Th-cell phenotype.

Indexed as

Enterovirus B, HumanAdoptive TransferAnimalsCD4-Positive T-LymphocytesCoxsackievirus InfectionsCytokinesDNA-Binding ProteinsImmunophenotypingLymphocyte DepletionMaleMiceMice, Inbred BALB CMyocarditisReceptors, Antigen, T-Cell, gamma-deltaSTAT4 Transcription FactorSTAT6 Transcription FactorCytokinesDNA-Binding ProteinsReceptors, Antigen, T-Cell, gamma-deltaStat4 protein, mouseSTAT4 Transcription FactorStat6 protein, mouseSTAT6 Transcription FactorTrans-Activators

Identifiers

PMID11390587
PMCPMC114301
OpenAlexW2100267450

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.