Department of Immunology, Tufts University School of Medicine, Boston, Massachusetts.
Department of Immunology, Tufts University School of Medicine, Boston, Massachusetts; Sackler School for Graduate Studies Immunology Program, Tufts University School of Medicine, Boston, Massachusetts.
Am J Pathol. 2019 Aug;189(8):1482-1494. doi: 10.1016/j.ajpath.2019.04.009. Epub 2019 May 18.
Heart failure (HF) has been traditionally viewed as a disease of the cardiac muscle associated with systemic inflammation. Burgeoning evidence implicates immune effector mechanisms that include immune cell activation and trafficking to the heart. Immune cell infiltration in the myocardium can have adverse effects in the heart and contribute to the pathogenesis of HF. Both innate and adaptive immunity operate sequentially, and the specificity of these responses depends on the initial trigger sensed by the heart. Although the role of the immune system in the initial inflammatory response to infection and injury is well studied, what sets the trajectory to HF from different etiologies and the role of immunity once HF has been established is less understood. Herein, we review experimental and clinical knowledge of cardiac inflammation induced by different triggers that often result in HF from different etiologies. We focus on the mechanisms of immune cell activation systemically and on the pathways immune cells use to traffic to the heart.
心力衰竭(HF)传统上被视为一种与全身炎症相关的心肌疾病。越来越多的证据表明,免疫效应机制包括免疫细胞的激活和向心脏的迁移。心肌中的免疫细胞浸润会对心脏产生不良影响,并导致心力衰竭的发病机制。先天免疫和适应性免疫依次发挥作用,这些反应的特异性取决于心脏感知到的初始触发因素。尽管免疫系统在感染和损伤的初始炎症反应中的作用已得到充分研究,但不同病因导致心力衰竭的轨迹以及心力衰竭一旦发生后免疫的作用仍知之甚少。在此,我们综述了不同触发因素引起的心脏炎症的实验和临床知识,这些触发因素通常会导致不同病因的心力衰竭。我们重点讨论了系统中免疫细胞激活的机制以及免疫细胞迁移到心脏的途径。