Abstract
The increased BAFF expression in B-cells of patients with systemic lupus erythematosus (SLE) is associated with B-cell hyperstimulation and T-cell hyperactivity, but the underlying mechanisms are still unclear. This study aimed to uncover the mechanisms that regulate the BAFF expression in SLE B-cells. The results demonstrated that the expression of miR-152-3p was significantly increased in SLE B-cells compared with normal controls. This study confirmed that Kruppel-like factor 5 (KLF5) was a direct target of miR-152-3p, and it could bind to the promoter region of BAFF and inhibit its expression in B-cells. The upregulation of miRNA-152-3p expression decreased the KLF5 expression and increased the BAFF expression in SLE B-cells. Knockdown of miR-152-3p expression inhibited the self-reactivity of SLE B-cells, thereby reducing the autoantibody production. The increased miR-152-3p expression in SLE B-cells led to an increase in BAFF expression by inhibiting KLF5 expression. These factors caused B-cell self-reactivity and autoantibody production, allowing participation in the disease process of SLE.
Highlights
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease that manifests multiple B cell abnormalities including amplification of memory B cells and increased levels of autoantibodies
A high-throughput miRNA microarray of the activities of 371 miRNAs isolated from B-cells of healthy controls and patients with active systemic lupus erythematosus (SLE) was conducted in a previous study [4]
Compared with Bcells transfected with scrambled sequence control, there was a significant increase in the expression levels of CD40, CD80, CD86 and miR-152-3p in B-cells transfected with miR-152-3p agomir (Figures 2A–C,G,H)
Summary
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease that manifests multiple B cell abnormalities including amplification of memory B cells and increased levels of autoantibodies. This subsequently affects multiple organs and systems, causing significant morbidity and mortality [1]. According to a previous study, the expression levels of 371 miRNAs in B-cells were altered in patients with active SLE than in healthy controls by high-throughput miRNA microarray. Among the 371 miRNAs, the Excessive miR-152-3p in SLE B-Cells miR-1246 expression level was reduced significantly in the Bcells of patients with active SLE. The miRNA microarray results showed that the miR-152-3p expression level was increased significantly in Bcells of patients with active SLE. Little is known with regard to the role of miR-152-3p in the function of B-cells and the pathogenesis of autoimmune diseases
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