The Immune System, An Arrow into the Heart. Principles of Cardioimmunology, An Emerging Branch in Medicine

医学 箭头 免疫系统 重症监护医学 免疫学 计算机科学 程序设计语言
作者
Carlo Caiati,Emilio Jirillo
出处
期刊:Current Vascular Pharmacology [Bentham Science Publishers]
卷期号:23 (3): 162-171 被引量:7
标识
DOI:10.2174/0115701611325234241202073459
摘要

Cardioimmunology is an emerging branch of medicine whose development has been facilitated by more sophisticated diagnostic procedures. Recent studies have mainly focused on the immune response during myocardial infarction (MI), and there is evidence that both resident and external immune cells participate in acute inflammatory disease, as well as tissue remodeling. Following MI, macrophages, dendritic cells (DCs) and mast cells (MCs) are the main players in the heart. Under steady-state conditions, cardiac resident macrophages (CRMs) protect the heart against stress and infectious events, being involved in cell and matrix turnover, as well as phagocytosis of apoptotic cells. Moreover, CRMs contribute to the resolution of inflammation via release of interleukin (IL)-10, and efferocytosis of dying cells. Conversely, CCR2+ monocytederived macrophages promote inflammation in the acute phase of myocardial damage, with the release of pro-inflammatory cytokines. Conventional (c) DCs possess enhanced capacity to present antigens to T lymphocytes. In MI patient autopsies, massive infiltration of T helper (Th) cells and CDs has been detected in the myocardium. Cardiac MCs play a dual role during MI, with the production of cytokines for early inflammatory response, and the release of anti-inflammatory cytokines, IL10 and IL-13 during the resolution phase. In experimental coronary artery ligation, the myocardium is infiltrated with Th1, Th2, Th17, and T regulatory (TREG) cells, which participate in the acute inflammation. In cardiac repair, T cell reparative response is mediated by TREG cells, with improved ventricular remodeling and function post-ischemia. In this review, emphasis will be placed on the innate and adaptive immune response during and post-MI. At the same time, immunotherapy- based cardiac failure following chimeric antigen receptor T-cell and immune checkpoint inhibitory therapy will be pointed out.
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