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心肌炎的免疫发病机制:心脏成纤维细胞、树突状细胞、巨噬细胞与CD4+ T细胞之间的相互作用

Immunopathogenesis of Myocarditis: The Interplay Between Cardiac Fibroblast Cells, Dendritic Cells, Macrophages and CD4+ T Cells.

作者信息

Amoah B Prince, Yang H, Zhang P, Su Z, Xu H

机构信息

Department of Immunology, School of Medical Science and Laboratory Medicine, Jiangsu University, Zhenjiang, China.

Department of Biomedical and Forensic Sciences, School of Biological Sciences, University of Cape Coast, Cape Coast, Ghana.

出版信息

Scand J Immunol. 2015 Jul;82(1):1-9. doi: 10.1111/sji.12298.

DOI:10.1111/sji.12298
PMID:25845946
Abstract

The myocardium responds to aetiologically different pathological injuries through a common multistep process involving highly co-ordinated interactions between cardiac and immune cells. Cardiac fibroblast cells which constitute the prevalent cell type in the heart to have their functional effects that express contractile proteins and exhibit increased migratory, proliferative and secretory properties. During the pathogenesis of myocarditis, cardiac fibroblast, dendritic cells, macrophages, CD4(+) T cells and other immune cells are known to play variable roles. It is becoming increasingly clear that cardiac fibroblasts are not passive players in immune responses, and several evidences show this through the release of soluble signals and/or direct interactions with these immune cells. Typically, fibroblasts are involved in synthesizing factors such as cytokines, chemokines, prostanoids, matrix components and matrix-degrading enzymes to influence dendritic cells, CD4(+) T cells and macrophage functions and vice versa in the pathogenesis of myocarditis. Again, evidence proves a crosstalk between cardiac fibroblasts and immune cells recruited into the myocardium during myocarditis in the microenvironments. This piece reviews the properties and roles of cardiac fibroblast cells, dendritic cells, macrophages and CD4(+) T cells in the pathogenesis of myocarditis, and how these cells interplay on each other in the microenvironment.

摘要

心肌通过一个共同的多步骤过程对病因不同的病理损伤作出反应,该过程涉及心脏细胞与免疫细胞之间高度协调的相互作用。心脏成纤维细胞是心脏中占主导地位的细胞类型,具有表达收缩蛋白以及迁移、增殖和分泌特性增加等功能效应。在心肌炎发病过程中,已知心脏成纤维细胞、树突状细胞、巨噬细胞、CD4(+) T细胞和其他免疫细胞发挥着不同作用。越来越清楚的是,心脏成纤维细胞在免疫反应中并非被动参与者,一些证据通过可溶性信号的释放和/或与这些免疫细胞的直接相互作用表明了这一点。通常,成纤维细胞参与合成细胞因子、趋化因子、前列腺素、基质成分和基质降解酶等因子,以影响树突状细胞、CD4(+) T细胞和巨噬细胞的功能,反之亦然,在心肌炎发病过程中。同样,有证据证明在心肌炎微环境中,心脏成纤维细胞与募集到心肌中的免疫细胞之间存在相互作用。本文综述了心脏成纤维细胞、树突状细胞、巨噬细胞和CD4(+) T细胞在心肌炎发病机制中的特性和作用,以及这些细胞在微环境中如何相互作用。

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