Key result
Distinct gamma-delta T-cell subsets control myocarditis susceptibility, with Vgamma1+ cells suppressing and Vgamma4+ cells promoting disease through their respective cytokine production.
Why the study?
Does depletion or adoptive transfer of specific Vγ+ T-cell subsets alter CD4+ Th-cell phenotype and prevent or enhance CVB3-induced myocarditis in BALB/c mice?
Population
Male BALB/cJ, BALB/c-Stat4tmI Gru, and BALB/c-Stat6tmI Gru mice, 5 to 6 weeks of age.
Comparison
Intraperitoneal injection of 10^4 PFU of… vs Uninfected mice, intravenous injection of 300 μg…
Design
Preclinical
Follow-up
7 days
Authors
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No immediate clinical implications from murine data; extends mechanistic understanding of γδ T-cell subsets in viral myocarditis.
Does depletion or adoptive transfer of specific Vγ+ T-cell subsets alter CD4+ Th-cell phenotype and prevent or enhance CVB3-induced myocarditis in BALB/c mice?
Distinct γδ T-cell subsets control susceptibility to viral myocarditis by biasing the CD4+ Th-cell response through specific cytokine production.
Huber et al. (2001) studied Coxsackievirus B3-induced myocarditis. Vgamma1+ and Vgamma4+ T-cell depletion or adoptive transfer vs. Hamster IgG or PBS was evaluated on Myocardial inflammation (% of myocardium inflamed). Distinct gamma-delta T-cell subsets control myocarditis susceptibility, with Vgamma1+ cells suppressing and Vgamma4+ cells promoting disease through their respective cytokine production.
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