Abstract
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.
Highlights
Systemic lupus erythematosus (SLE) is an autoimmune disease that causes multiple organ damage in women of childbearing age and has a relapsing-remitting course
One and 2 occur mainly in the central nervous system, while 3 and 4 occur mainly in the periphery [15]. In autoimmune diseases such as SLE, self-tolerance may be disrupted by environmental factors such as viruses, in addition to genetic predisposition, with activation, proliferation, class switching, and antibody production possibly induced by external factors other than B-cells, such as dendritic cells and Th cells, as well as by endogenous dysfunction of B-cells themselves
We have reported that activated memory B-cells [IgD-CD27double-negative (DN) memory, class-switched memory B-cells], and plasmablasts are deeply involved in the pathogenesis of SLE [19]
Summary
First Department of Internal Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan. Reviewed by: Zheng Wei, Yale University, United States Michelle Swanson-Mungerson, Midwestern University, United States. Specialty section: This article was submitted to Rheumatology, a section of the journal
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