Belyaeva Irina V, Kosova Anna N, Vasiliev Andrei G
Department of Pathophysiology, St. Petersburg State Pediatric Medical University, Ministry of Healthcare of the Russian Federation, 194100 Saint Petersburg, Russia.
Pathophysiology. 2022 Jun 13;29(2):298-318. doi: 10.3390/pathophysiology29020022.
Tuberculosis remains a common and dangerous chronic bacterial infection worldwide. It is long-established that pathogenesis of many autoimmune diseases is mainly promoted by inadequate immune responses to bacterial agents, among them Mycobacterium tuberculosis. Tuberculosis is a multifaceted process having many different outcomes and complications. Autoimmunity is one of the processes characteristic of tuberculosis; the presence of autoantibodies was documented by a large amount of evidence. The role of autoantibodies in pathogenesis of tuberculosis is not quite clear and widely disputed. They are regarded as: (1) a result of imbalanced immune response being reactive in nature, (2) a critical part of TB pathogenicity, (3) a beginning of autoimmune disease, (4) a protective mechanism helping to eliminate microbes and infected cells, and (5) playing dual role, pathogenic and protective. There is no single autoimmunity-mechanism development in tuberculosis; different pathways may be suggested. It may be excessive cell death and insufficient clearance of dead cells, impaired autophagy, enhanced activation of macrophages and dendritic cells, environmental influences such as vitamin D insufficiency, and genetic polymorphism, both of and host.
结核病在全球范围内仍然是一种常见且危险的慢性细菌感染。长期以来，许多自身免疫性疾病的发病机制主要是由对包括结核分枝杆菌在内的细菌病原体的免疫反应不足所推动的。结核病是一个多方面的过程，有许多不同的结果和并发症。自身免疫是结核病的特征性过程之一；大量证据证明了自身抗体的存在。自身抗体在结核病发病机制中的作用尚不完全清楚，且存在广泛争议。它们被认为是：（1）免疫反应失衡的结果，本质上具有反应性；（2）结核病致病性的关键部分；（3）自身免疫性疾病的开端；（4）一种有助于清除微生物和感染细胞的保护机制；（5）发挥致病和保护的双重作用。结核病中不存在单一的自身免疫机制发展过程；可能存在不同的途径。这可能是细胞过度死亡和死亡细胞清除不足、自噬受损、巨噬细胞和树突状细胞的激活增强、环境影响如维生素D缺乏以及宿主和病原体的基因多态性。
