ArticleJournal of virology2002
Vgamma4(+) T cells promote autoimmune CD8(+) cytolytic T-lymphocyte activation in coxsackievirus B3-induced myocarditis in mice: role for CD4(+) Th1 cells.
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 40 papers.
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.
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.
Who cites it
40 citing papers in PubMed, 105 citations in OpenAlex.
- The knowns and unknowns of cardiac autoimmunity in viral myocarditis.Reviews in medical virology · 2023Review
- Coxsackievirus B3 elicits a sex-specific CD8+ T cell response which protects female mice.PLoS pathogens · 2023Article
- A combination ofExperimental and therapeutic medicine · 2023Article
- A viral-specific CD4Frontiers in immunology · 2023Article
- Review
- Programmed Cell Death-1: Programmed Cell Death-Ligand 1 Interaction Protects Human Cardiomyocytes Against T-Cell Mediated Inflammation and Apoptosis Response In Vitro.International journal of molecular sciences · 2020Article
- Assessment of Thymic Output Dynamics AfterFrontiers in immunology · 2020Article
- Myocarditis in Humans and in Experimental Animal Models.Frontiers in cardiovascular medicine · 2019Review
- Gr-1+ Cells Other Than Ly6G+ Neutrophils Limit Virus Replication and Promote Myocardial Inflammation and Fibrosis Following Coxsackievirus B3 Infection of Mice.Frontiers in cellular and infection microbiology · 2018Article
- The adaptive immune response to cardiac injury-the true roadblock to effective regenerative therapies?NPJ Regenerative medicine · 2017Review
- Increased frequency of follicular helper T cells in mice viral myocarditis is relevant with anti-ANT antoantibody.Virology journal · 2015Article
- γδ T Cells and NK Cells - Distinct Pathogenic Roles as Innate-Like Immune Cells in CNS Autoimmunity.Frontiers in immunology · 2015Review
- Galectin-9 induced myeloid suppressor cells expand regulatory T cells in an IL-10-dependent manner in CVB3-induced acute myocarditis.International journal of molecular sciences · 2014Article
- Global characterization of differential gene expression profiles in mouse Vγ1+ and Vγ4+ γδ T cells.PloS one · 2014Article
- c-FLIP-Short reduces type I interferon production and increases viremia with coxsackievirus B3.PloS one · 2014Article
- Ex vivo analysis of resident hepatic pro-inflammatory CD1d-reactive T cells and hepatocyte surface CD1d expression in hepatitis C.Journal of viral hepatitis · 2013Article
- Cross-regulation of T regulatory-cell response after coxsackievirus B3 infection by NKT and γδ T cells in the mouse.The American journal of pathology · 2013Article
- Article
- Sex-specific signaling through Toll-Like Receptors 2 and 4 contributes to survival outcome of Coxsackievirus B3 infection in C57Bl/6 mice.Biology of sex differences · 2012Article
- Update on coxsackievirus B3 myocarditis.Current opinion in rheumatology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
T cells expressing the Vgamma4 T-cell receptor (TCR) promote myocarditis in coxsackievirus B3 (CVB3)-infected BALB/c mice. CD1, a major histocompatibility complex (MHC) class I-like molecule, is required for activation of Vgamma4(+) cells. Once activated, Vgamma4(+) cells initiate myocarditis through gamma interferon (IFN-gamma)-mediated induction of CD4(+) T helper type 1 (Th1) cells in the infected animal. These CD4(+) Th1 cells are required for activation of an autoimmune CD8(+) alphabeta TCR(+) effector, which is the predominant pathogenic agent in this model of CVB3-induced myocarditis. Activated Vgamma4(+) cells can adoptively transfer myocarditis into BALB/c mice infected with a nonmyocarditic variant of CVB3 (H310A1) but cannot transfer myocarditis into either uninfected or CD1(-/-) recipients, demonstrating the need for both infection and CD1 expression for Vgamma4(+) cell function. In contrast, CD8(+) alphabeta TCR(+) cells transfer myocarditis into either infected CD1(-/-) or uninfected recipients, showing that once activated, the CD8(+) alphabeta TCR(+) effectors function independently of both virus and CD1. Vgamma4(+) cells given to mice lacking CD4(+) T cells minimally activate the CD8(+) alphabeta TCR(+) cells. These studies show that Vgamma4(+) cells determine CVB3 pathogenicity by their ability to influence both the CD4(+) and CD8(+) adaptive immune response. Vgamma4(+) cells enhance CD4(+) Th1 (IFN-gamma(+)) cell activation through IFN-gamma- and CD1-dependent mechanisms. CD4(+) Th1 cells promote activation of the autoimmune CD8(+) alphabeta TCR(+) effectors.
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What OpenQuestion holds
Registered trials
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.