Developing successful immunomodulatory therapies against ventricular remodeling after myocardial infarction

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Left ventricular (LV) remodeling leads to chronic heart failure and is a main determinant of morbidity and mortality after myocardial infarction (MI). Mice with DC ablation showed deteriorated LV function and remodeling concomitant with enhanced expression of IL-1beta, IL-18, and TNF-alpha, prolonged extracellular matrix degradation, marked infiltration of proinflammatory monocytes. A deficiency of gamma-delta T cells improved survival, limiting infarct expansion and fibrosis in noninfarcted myocardium and alleviating LV dilatation and systolic dysfunction after MI. IL-17A-producing gamma-delta T cells promotes sustained infiltration of neutrophils and macrophages, , aggravating cardiomyocyte death, and enhancing fibroblast proliferation. Depletion of NK cells from mice exhibited severe respiratory. Adoptive transfer of NK cells from wild-type mice, but not from IL-10 knockout mice, into the NK cell-depleted mice rescued the respiratory phenotype.