Key result
IL-12 deficiency in mice did not prevent CVB3-induced myocarditis but significantly increased viral replication and decreased macrophage and neutrophil populations in the heart.
Why the study?
Does IL-12 deficiency affect the development of CVB3-induced myocarditis and viral replication in mice?
Population
Mice deficient in IL-12p35, TNFRp55, STAT4, or IFN-gamma, and wild-type BALB/c controls, infected with…
Comparison
Genetic deficiency of IL-12p35, TNFRp55, STAT4… vs Wild-type BALB/c controls
Design
Preclinical
Authors
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Caution against Th1-suppressing therapies in viral myocarditis; leaves open IL-12 role in human disease.
Does IL-12 deficiency affect the development of CVB3-induced myocarditis and viral replication in mice?
The IL-12/STAT4 pathway of IFN-gamma production is important in limiting CVB3 replication, suggesting that therapies reducing Th1 responses may exacerbate viral myocarditis.
Fairweather et al. (2005) studied Coxsackievirus B3 (CVB3)-induced myocarditis. IL-12 deficiency (IL-12p35 knockout) vs. Wild-type BALB/c controls was evaluated on Myocarditis development and viral replication. IL-12 deficiency in mice did not prevent CVB3-induced myocarditis but significantly increased viral replication and decreased macrophage and neutrophil populations in the heart.
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