Memory B cells are increased in systemic lupus erythematosus (SLE) cases, but the qualitative abnormalities and induction mechanism of these cells are unclear. Here, we subclassified B cells by their chemokine receptor expression and investigated their induction mechanism. The peripheral blood of patients with SLE showed higher levels of CXCR5- and CXCR3+ B cells. CXCR5-CXCR3+ B cell levels were elevated in patients with active SLE, which decreased with improving disease conditions. Interferon (IFN)-γ stimulation increased CXCR3 expression, whereas IFN-β stimulation reduced CXCR5 expression in B cells. Furthermore, CXCR5-CXCR3+ B cells were induced by a combination of IFN-β and IFN-γ stimulation. Renal tissue examination of patients with active lupus nephritis confirmed the presence of CD19+CXCR3+ B cells. Collectively, the results revealed qualitative abnormalities accompanying reduced CXCR5 expression via type I IFN and enhanced CXCR3 expression via type II IFN in SLE, suggesting their involvement in B cell infiltration into tissues and inflammatory pathogenesis.

中文翻译：

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I型和II型干扰素导致系统性红斑狼疮患者B细胞趋化因子受体异常表达。

系统性红斑狼疮（SLE）病例中的记忆B细胞增加，但这些细胞的质性异常和诱导机制尚不清楚。在这里，我们通过趋化因子受体的表达将B细胞细分为亚类，并研究其诱导机制。SLE患者的外周血显示较高水平的CXCR5-和CXCR3 + B细胞。活动性SLE患者的CXCR5-CXCR3 + B细胞水平升高，随着疾病状况的改善而降低。干扰素（IFN）-γ刺激可增加CXCR3表达，而IFN-β刺激可降低B细胞中CXCR5表达。此外，通过结合IFN-β和IFN-γ刺激来诱导CXCR5-CXCR3 + B细胞。活动性狼疮性肾炎患者的肾脏组织检查证实存在CD19 + CXCR3 + B细胞。总的来说，