Key result
Infection with the H310A1 coxsackievirus B3 variant or T-cell depletion reduced heart size and cardiac inflammation in TNF1.6 mice by activating CD4+CD25+FoxP3+ T regulatory cells.
Why the study?
Does infection with coxsackievirus B3 variant H310A1 or T-cell depletion reduce cardiomyopathy in TNF-alpha transgenic mice?
Population
Transgenic mice expressing the tumor necrosis factor-alpha gene under the cardiac myosin promoter that…
Comparison
Infection with coxsackievirus B3 variant H310A1… vs Control TNF1.6 mice
Design
Preclinical
Authors
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May attenuate TNF-driven cardiomyopathy via Tregs in mice; hypothesis-generating for human translation.
Does infection with coxsackievirus B3 variant H310A1 or T-cell depletion reduce cardiomyopathy in TNF-alpha transgenic mice?
T regulatory cells induced by a specific coxsackievirus B3 variant can abrogate autoimmunity and cardiomyopathy caused by TNF-alpha overexpression in a mouse model.
Huber et al. (2006) studied Dilated cardiomyopathy. Coxsackievirus B3 (CVB3) variant H310A1 or T-cell depletion vs. Control TNF1.6 mice was evaluated on Heart size, plasma troponin I concentrations, and cardiac inflammation. Infection with the H310A1 coxsackievirus B3 variant or T-cell depletion reduced heart size and cardiac inflammation in TNF1.6 mice by activating CD4+CD25+FoxP3+ T regulatory cells.
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