METHODS: Cytokines of EBV-infected SLE patients were measured by ELISA and assessed in conjunction with their clinical data. IFN-α, c-Maf, and the differentiation of Th17/Treg cells in SLE patients and MRL/LPR mice were analyzed using FCM, WB, RT-PCR, etc. Following the infection of cells and mice with EBV or viral mimic poly (dA:dT), the changes of the aforementioned indicators were investigated. The relationship among IFN-α, STAT3, c-Maf and Th17 cells was determined by si-RNA technique.
RESULTS: Many SLE patients are found to be complicated by viral infections; Further, studies have demonstrated that viral infection, especially EBV, is involved in SLE development. This study showed that viral infections might promote IFN-α secretion, inhibit c-Maf expression by activating STAT3, increase Th17 cell differentiation, and lead to the immune imbalance of Th17/Treg cells, thus playing a role in the onset and progression of SLE.
CONCLUSIONS: This study demonstrates that EBV infections may contribute to SLE development by activating STAT3 through IFN-α, inhibiting c-Maf, and causing Th17/Treg immune imbalance. Our work provided a new insight into the pathogenesis and treatment of SLE.
方法:通过ELISA测定EBV感染的SLE患者的细胞因子,并结合其临床数据进行评估。IFN-α,c-Maf,用FCM分析SLE患者和MRL/LPR小鼠Th17/Treg细胞的分化,WB,RT-PCR,等。用EBV或病毒模拟物poly(dA:dT)感染细胞和小鼠后,调查了上述指标的变化。IFN-α,通过si-RNA技术测定STAT3、c-Maf和Th17细胞。
结果:发现许多SLE患者并发病毒感染;研究表明,病毒感染,尤其是EBV,参与SLE开发。这项研究表明,病毒感染可能促进IFN-α的分泌,通过激活STAT3抑制c-Maf表达,增加Th17细胞分化,导致Th17/Treg细胞免疫失衡,从而在SLE的发病和进展中发挥作用。
结论:这项研究表明,EBV感染可能通过IFN-α激活STAT3促进SLE的发展,抑制c-Maf,并导致Th17/Treg免疫失衡。我们的工作为SLE的发病机制和治疗提供了新的见解。