Regulation of B-cell function by miRNAs impacting Systemic lupus erythematosus progression
Bitang Huang, Fengbiao Guo, Jiaxuan Chen, Ling Lu, Shenglan Gao, Chunlong Yang, Han Wu, Wenying Luo, Qingjun Pan
Abstract
• miRNAs are critical regulators in SLE, offering diagnostic and therapeutic strategies. • miRNAs interact with DNA methylation, which is crucial in SLE pathogenesis and therapy. • miRNAs regulate cytokines, autophagy, and signaling pathways in SLE. • miRNAs influence B cell development; targeting them offers therapeutic potential. • miRNAs modulate B cell function in SLE, impacting disease progression and treatment. Systemic lupus erythematosus (SLE) is a complex autoimmune disease marked by abnormal B-cell proliferation and increased autoantibodies. miRNAs play a crucial role in regulating B-cell dysfunction and SLE pathology. miRNAs influence DNA methylation, B-cell activation, and gene expression, contributing to SLE pathogenesis. miRNAs impact B cells through key processes like proliferation, differentiation, tolerance, and apoptosis. miRNAs also exacerbate inflammation and immune responses by modulating Interleukin 4 (IL-4), IL-6, and interferon cytokines. Autophagy, a key degradation mechanism, is also regulated by specific miRNAs that impact SLE pathology. This article explores the role of multiple miRNAs in regulating B-cell development, proliferation, survival, and immune responses, influencing SLE pathogenesis. miRNAs like miR-23a, the miR-17 ∼ 92 family, and miR-125b/miR-221 affect B-cell development by regulating transcription factors, signaling pathways, and cell cycle genes. miRNAs such as miR-181a-5p and miR-23a-5p are differentially regulated across developmental stages, emphasizing their complex regulatory roles in B-cell biology. This article synthesizes miRNA-B cell interactions to offer new strategies and directions for SLE diagnosis and treatment.