Iwata Shigeru, Tanaka Yoshiya
First Department of Internal Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Front Med (Lausanne). 2022 Feb 25;9:849120. doi: 10.3389/fmed.2022.849120. eCollection 2022.
Systemic lupus erythematosus (SLE) is an autoimmune disease that causes multiple organ damage in women of childbearing age and has a relapsing-remitting course. SLE is caused by the interaction between genetic and environmental factors, however, its underlying triggers remain unknown. Among the environmental factors, the involvement of infections as a trigger for SLE, especially those of viral etiology, has been widely reported. Human endogenous retroviruses (HERVs) may put patients at a genetic predisposition to SLE, while the Epstein-Barr virus (EBV) may play a role as an environmental factor that triggers the development of SLE. It has been suggested that EBV-infected B-cells may become resistant to apoptosis, resulting in the activation, proliferation, and antibody production of autoreactive B-cells, which cause tissue damage in SLE. However, the interaction between the virus and immune cells, as well as the impact of the virus on the differentiation and dysfunction of immune cells, remain unclear. In this review, we focus on the relationship between the development and pathogenesis of SLE and viral infections, as well as the mechanism of SLE exacerbation via activation of immune cells, such as B-cells, based on the latest findings.
系统性红斑狼疮（SLE）是一种自身免疫性疾病，可导致育龄期女性多器官损害，且病程呈复发-缓解型。SLE由遗传因素和环境因素相互作用引起，但其潜在触发因素仍不明确。在环境因素中，感染作为SLE的触发因素，尤其是病毒病因的感染，已被广泛报道。人类内源性逆转录病毒（HERVs）可能使患者具有SLE的遗传易感性，而爱泼斯坦-巴尔病毒（EBV）可能作为触发SLE发生发展的环境因素发挥作用。有人提出，EBV感染的B细胞可能对凋亡产生抗性，导致自身反应性B细胞活化、增殖并产生抗体，从而在SLE中引起组织损伤。然而，病毒与免疫细胞之间的相互作用，以及病毒对免疫细胞分化和功能障碍的影响仍不清楚。在本综述中，我们基于最新研究结果，重点探讨SLE的发生发展及发病机制与病毒感染之间的关系，以及通过激活免疫细胞（如B细胞）导致SLE病情加重的机制。
