Role of CD4 T-cells for regulating splenic myelopoiesis and monocyte differentiation after experimental myocardial infarction.

Myocardial infarction (MI) induces the generation of proinflammatory Ly6C monocytes in the spleen and the recruitment of these cells to the myocardium. CD4 Foxp3 CD25 T-cells (Tregs) promote the healing process after myocardial infarction by engendering a pro-healing differentiation state in myocardial monocyte-derived macrophages. We aimed to study the effects of CD4 T-cells on splenic myelopoiesis and monocyte differentiation.

Myocardial aging as a T-cell-mediated phenomenon.

In recent years, the myocardium has been rediscovered under the lenses of immunology, and lymphocytes have been implicated in the pathogenesis of cardiomyopathies with different etiologies. Aging is an important risk factor for heart diseases, and it also has impact on the immune system. Thus, we sought to determine whether immunological activity would influence myocardial structure and function in elderly mice.

CD4 Foxp3 T-cells contribute to myocardial ischemia-reperfusion injury.

Objective: The present study analyzed the effect of CD4 Forkhead box protein 3 negative (Foxp3) T-cells and Foxp3 CD4 T-cells on infarct size in a mouse myocardial ischemia-reperfusion model.

Approach And Results: We examined the infarct size as a fraction of the area-at-risk as primary study endpoint in mice after 30minutes of coronary ligation followed by 24hours of reperfusion. CD4 T-cell deficient MHC-II KO mice showed smaller histologically determined infarct size (34.