Pathomechanisms of Immunosenescence in the post-myocardial infarction healing response (A3)

The prevalence of myocardial diseases increases sharply with age, but most preclinical research in cardiology is conducted in young, healthy animals. Aging is accompanied by accumulating effector T-cells with an inflammatory phenotype that can affect the post- myocardial infarction (MI) healing process. Herein, we will employ several experimental in vivo models to dissect the mechanisms through which immune status alterations associated with aging, and particularly T-cell immunosenescence, impact the post-MI outcome and the progression of ischemic heart failure.

Immunosenescence and T-Lymphozyten

Life expectancy has risen steadily over the past century, as has the occurrence of age-related diseases, such as MI and heart failure (HF). Aging is often accompanied by increased low-grade chronic inflammation and accumulated interferon-gamma (IFN-γ)-producing effector T-cells with proinflammatory and cytotoxic functions. These systemic alterations in the aging T-cell compartment impact myocardial physiology, individual susceptibility to heart diseases and long-term prognoses.

Rationale and aims

Our overarching hypothesis is that the immunosenescence profile, marked by clonal expansions of IFN-γ-pro- ducing T-cells and a decline in the naïve T-cell pool, impacts the post-MI healing potential and accelerates the development of ischemic heart failure.