The Immune System: An Arrow to the Heart and Principles of Cardioimmunology as an Emerging Branch of Medicine.

IF 2.8 3区 医学 Q2 PERIPHERAL VASCULAR DISEASE Current vascular pharmacology Pub Date : 2025-01-10 DOI:10.2174/0115701611325234241202073459
Carlo Caiati, Emilio Jirillo
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Abstract

Background: 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. Cardiac Innate Immune Cells: 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+ monocyte-derived 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. Adaptive Immune Response: 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.

Specific aims: 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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免疫系统:心脏之箭》和《作为新兴医学分支的心脏免疫学原理》。
背景:心脏免疫学是一门新兴的医学分支,它的发展已经被更复杂的诊断程序所促进。近年来的研究主要集中在心肌梗死(MI)期间的免疫反应,有证据表明,常驻免疫细胞和外部免疫细胞都参与了急性炎症性疾病以及组织重塑。心脏先天免疫细胞:心肌梗死后,巨噬细胞、树突状细胞(dc)和肥大细胞(MCs)是心脏的主要参与者。在稳态条件下,心脏巨噬细胞(CRMs)保护心脏免受应激和感染事件的影响,参与细胞和基质的更新,以及凋亡细胞的吞噬。此外,crm通过释放白细胞介素(IL)-10和垂死细胞的efferocytosis,有助于炎症的消退。相反,CCR2+单核细胞来源的巨噬细胞在心肌损伤的急性期促进炎症,释放促炎细胞因子。常规(c) dc向T淋巴细胞呈递抗原的能力增强。在心肌梗死患者的尸检中,发现心肌中有大量辅助性T细胞(Th)和cd浸润。心肌MCs在心肌梗死过程中发挥双重作用,既产生早期炎症反应所需的细胞因子,又在缓解期释放抗炎细胞因子、il - 10和IL-13。适应性免疫反应:实验性冠状动脉结扎术中,心肌浸润Th1、Th2、Th17和T调节(TREG)细胞,参与急性炎症反应。在心脏修复中,T细胞的修复反应是由TREG细胞介导的,缺血后心室重构和功能得到改善。具体目的:在这篇综述中,重点将放在先天性和适应性免疫反应期间和后心肌梗死。同时,将指出嵌合抗原受体t细胞和免疫检查点抑制治疗后以免疫治疗为基础的心力衰竭。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Current vascular pharmacology
Current vascular pharmacology 医学-外周血管病
CiteScore
9.20
自引率
4.40%
发文量
54
审稿时长
6-12 weeks
期刊介绍: Current Vascular Pharmacology publishes clinical and research-based reviews/mini-reviews, original research articles, letters, debates, drug clinical trial studies and guest edited issues to update all those concerned with the treatment of vascular disease, bridging the gap between clinical practice and ongoing research. Vascular disease is the commonest cause of death in Westernized countries and its incidence is on the increase in developing countries. It follows that considerable research is directed at establishing effective treatment for acute vascular events. Long-term treatment has also received considerable attention (e.g. for symptomatic relief). Furthermore, effective prevention, whether primary or secondary, is backed by the findings of several landmark trials. Vascular disease is a complex field with primary care physicians and nurse practitioners as well as several specialties involved. The latter include cardiology, vascular and cardio thoracic surgery, general medicine, radiology, clinical pharmacology and neurology (stroke units).
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