Kurrer Michael O, Kopf Manfred, Penninger Josef M, Eriksson Urs
Department of Pathology, University Hospital, Zurich, Switzerland.
Swiss Med Wkly. 2002 Jul 27;132(29-30):408-13. doi: 10.4414/smw.2002.10054.
A growing body of evidence suggests that autoimmune responses are involved in the pathogenesis of myocarditis and postinfectious cardiomyopathy. Autoimmunity may also arise after ischaemic or traumatic damage to heart tissue. Myocarditis leading to heart failure can be mimicked in rodents by immunisation with cardiac alpha myosin and peptides derived from it. Cytokines and chemokines, produced mainly by T-cells and antigen-presenting cells, control immune responses by acting as either potentiating or inhibitory agents. Gene targeting and experiments with antibodies and/or antagonists blocking cytokines and their receptors have uncovered mechanisms whereby such regulatory molecules are involved in the pathogenesis of myocarditis. Identification of regulatory key cytokines and the associated pro- or anti-inflammatory pathways involved in the pathogenesis of cardiac inflammation may have important implications for therapeutic strategies and vaccine design in the future.
越来越多的证据表明,自身免疫反应参与了心肌炎和感染后心肌病的发病机制。心脏组织发生缺血或创伤性损伤后也可能出现自身免疫。通过用心脏α-肌球蛋白及其衍生肽进行免疫接种,可在啮齿动物中模拟导致心力衰竭的心肌炎。主要由T细胞和抗原呈递细胞产生的细胞因子和趋化因子,通过作为增强剂或抑制剂来控制免疫反应。基因靶向以及使用抗体和/或拮抗剂阻断细胞因子及其受体的实验,揭示了这些调节分子参与心肌炎发病机制的机制。确定参与心脏炎症发病机制的关键调节细胞因子以及相关的促炎或抗炎途径,可能对未来的治疗策略和疫苗设计具有重要意义。