Adaptive immunity-driven inflammation and cardiovascular disease

Abstract

The adaptive immune response has recently emerged as an important factor in a wide variety of cardiovascular disorders including atherosclerosis, hypertension, cardiac remodeling, and heart failure; however, its role is not fully understood. Since an assortment of innate responsive cells, e.g., neutrophils and monocytes/macrophages, coordinate with adaptive immunity, e.g., T cells, dendritic cells, and B cells, the temporal response and descriptions pertinent to the cellular phenotype and inflammation processes, in general, need additional investigation, clarification, and consensus particularly in cardiovascular disease. This Perspectives article reviews the contributions of 15 articles (including 7 reviews) published in the American Journal of Physiology-Heart and Circulatory Physiology in response to the Call for Papers: Adaptive Immunity in Cardiovascular Disease. Here, we summarize the crucial reported findings at the cardiac, vascular, immune, and molecular levels and discuss the translational feasibility and benefits of future prospective research into the adaptive immune response. Readers are encouraged to evaluate the data and learn from this collection of novel studies.

Keywords: adaptive immunity; atherosclerosis; eosinphilia; hypertension; myocardial infarction.

Fig. 1.

The physiological and pathological oscillation of the adaptive immune response in cardiovascular disease is not fully understood. Response to a trigger, e.g., endothelial injury, myocyte death, or vascular injury/stress, initiates activation of the immune response, i.e., monocytes/macrophages, T cells, and B cells. Normal physiological response would be to dampen/resolve inflammation after the clearance of the trigger. A failure to initiate the adaptive immune response is what leads to the chronic inflammatory state, often resulting in cardiovascular pathology such as atherosclerosis, heart failure, and hypertension.