ArticleThe American journal of pathology2013
Cross-regulation of T regulatory-cell response after coxsackievirus B3 infection by NKT and γδ T cells in the mouse.
Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 23 citations in OpenAlex.
- The gut virome and regulatory T cell axis in health and systemic disease.Microbiome research reports · 2026Review
- γδ T Cells Mediate a Requisite Portion of a Wound Healing Response Triggered by Cutaneous Poxvirus Infection.Viruses · 2024Article
- Revisiting regulatory T cells as modulators of innate immune response and inflammatory diseases.Frontiers in immunology · 2023Review
- Electroimmunology and cardiac arrhythmia.Nature reviews. Cardiology · 2021Review
- Immunomodulatory Effects of Rhinovirus and Enterovirus Infections During the First Year of Life.Frontiers in immunology · 2020Article
- Myocarditis in Humans and in Experimental Animal Models.Frontiers in cardiovascular medicine · 2019Review
- T-cell immunity in myocardial inflammation: pathogenic role and therapeutic manipulation.British journal of pharmacology · 2017Review
- Age-Associated Changes in Estrogen Receptor Ratios Correlate with Increased Female Susceptibility to Coxsackievirus B3-Induced Myocarditis.Frontiers in immunology · 2017Review
- γδ T Cells and dendritic cells in refractory Lyme arthritis.Journal of leukocyte biology · 2015Review
- Organ-specific protective role of NKT cells in virus-induced inflammatory demyelination and myocarditis depends on mouse strain.Journal of neuroimmunology · 2015Article
- Nucleotide differences of coxsackievirus B3 and chronic myocarditis.Heart and vessels · 2015Article
- The role of myeloid cell activation and arginine metabolism in the pathogenesis of virus-induced diseases.Frontiers in immunology · 2014Review
- Learning from myocarditis: mimicry, chaos and black holes.F1000prime reports · 2014Review
- ERJournal of clinical & cellular immunologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Coxsackievirus B3 (CVB3) variants H3 and H310A1 differ by a single nonconserved amino acid in the VP2 capsid region. C57Bl/6 mice infected with the H3 virus develop myocarditis correlating with activation of T cells expressing the Vγ4 T cell receptor chain. Infecting mice with H310A1 activates natural killer T (NKT; mCD1d-tetramer(+) TCRβ(+)) cells, but not Vγ4 T cells, and fails to induce myocarditis. H310A1 infection preferentially activates M2 alternatively activated macrophage and CD4(+)FoxP3 (T regulatory) cells, whereas CD4(+)Th1 (IFN-γ(+)) cells are suppressed. By contrast, H3 virus infection activates M1 proinflammatory and CD4(+)Th1 cells, but not T regulatory cells. The M1 macrophage show significantly increased CD1d expression compared to M2 macrophage. The ability of NKT cells to suppress myocarditis was shown by adoptive transfer of purified NKT cells into H3-infected NKT knockout (Jα18 knockout) mice, which inhibited cardiac inflammation and increased T regulatory cell response. Cardiac virus titers were equivalent in all mouse strains indicating that neither Vγ4 nor NKT cells participate in control of virus infection. These data show that NKT and Vγ4 cells cross-regulate T regulatory cell responses during CVB3 infections and are the primary factor determining viral pathogenesis in this mouse model.
Indexed as
Identifiers
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.