Autoimmune diseases are characterized by circulating antibodies and immune complexes directed against self-tissues that result in both systemic and organ-specific inflammation and pathology. Most autoimmune diseases occur more often in women than men. One exception is myocarditis, which is an inflammation of the myocardium that is typically caused by viral infections. Sex differences in the immune response and the role of the sex hormones estrogen and testosterone are well established based on animal models of autoimmune viral myocarditis as well as in mitochondrial function leading to reactive oxygen species production. RNA viruses like coxsackievirus B3, the primary cause of myocarditis in the US, activate the inflammasome through mitochondrial antiviral signaling protein located on the mitochondrial outer membrane. Toll-like receptor 4 and the inflammasome are the primary signaling pathways that increase inflammation during myocarditis, which is increased by testosterone. This review describes what is known about sex differences in inflammation, redox biology and mitochondrial function in the male-dominant autoimmune disease myocarditis and highlights gaps in the literature and future directions.

自身免疫性疾病的特点是循环抗体和免疫复合物针对自身组织，导致全身和器官特异性炎症和病理。大多数自身免疫性疾病在女性中比男性更常见。一个例外是心肌炎，这是一种通常由病毒感染引起的心肌炎症。基于自身免疫性病毒性心肌炎的动物模型以及导致活性氧产生的线粒体功能，免疫反应以及性激素雌激素和睾酮的作用中的性别差异已得到充分证实。RNA 病毒（如柯萨奇病毒 B3）（美国心肌炎的主要原因）通过位于线粒体外膜上的线粒体抗病毒信号蛋白激活炎症小体。Toll 样受体 4 和炎症小体是心肌炎期间增加炎症的主要信号通路，睾酮会增加炎症。这篇综述描述了男性主导的自身免疫性疾病心肌炎中炎症、氧化还原生物学和线粒体功能的性别差异的已知情况，并强调了文献中的空白和未来的方向。