Key result
T helper cells with specificity for an antigen in cardiomyocytes accelerated the progression from hypertrophy to heart failure in response to pressure overload independently of autoantibodies.
Why the study?
Do T helper cells with specificity for an antigen in cardiomyocytes promote pressure overload-induced progression from hypertrophy to heart failure?
Population
Mice subjected to transverse aortic constriction to induce pressure overload, specifically comparing…
Comparison
Presence of cardiomyocyte-antigen-specific CD4+… vs cMy-mOVA mice subjected to TAC.
Design
Preclinical
Authors
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T-cell antigen specificity may accelerate HF in pressure overload; leaves open immunomodulatory targets in human disease.
Do T helper cells with specificity for an antigen in cardiomyocytes promote pressure overload-induced progression from hypertrophy to heart failure?
T helper cells specific to cardiomyocyte antigens can directly accelerate the progression of heart failure in response to pressure overload, independent of autoantibodies.
Gröschel et al. (2017) studied Pressure overload-induced heart failure (n=81). Presence of OVA-specific CD4+ T helper cells (cMy-mOVA-OT-II mice) with transverse aortic constriction vs. cMy-mOVA mice (lacking OVA-specific T cells) with transverse aortic constriction was evaluated on Progression to heart failure (ejection fraction and fractional area shortening). T helper cells with specificity for an antigen in cardiomyocytes accelerated the progression from hypertrophy to heart failure in response to pressure overload independently of autoantibodies.
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