The peripheral blood of systemic lupus erythematosus patients showed an increased expression of CXCR5 positive T cells. However, the molecular mechanism of the abnormal expression of CXCR5 in SLE CD4+ T cells remains unclear. The present study demonstrated that the levels of H3K4me3 and H3K36me3 in CXCR5 promoter were significantly higher in SLE patients than those in healthy controls. Furthermore, the expression of SETD3 was upregulated in SLE CD4+ T cells as compared to the healthy controls. Excessive SETD3 increased the level of H3K4me3 and H3K36me3 and promoted the expression of CXCR5. These data strongly suggested that SETD3 plays a major role in the regulation of CXCR5 expression and the progression of SLE.

中文翻译：

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过度表达SETD3导致SLE患者CD4+T细胞CXCR5的过表达。

系统性红斑狼疮患者外周血CXCR5阳性T细胞表达增加。然而，SLE CD4+ T细胞中CXCR5异常表达的分子机制尚不清楚。本研究表明，SLE 患者 CXCR5 启动子中 H3K4me3 和 H3K36me3 的水平显着高于健康对照组。此外，与健康对照相比，SLE CD4+ T 细胞中 SETD3 的表达上调。过量的SETD3增加H3K4me3和H3K36me3的水平并促进CXCR5的表达。这些数据强烈表明 SETD3 在 CXCR5 表达的调节和 SLE 的进展中起主要作用。