Abstract：
OBJECTIVE: Systemic lupus erythematosus (SLE) is a multi-organ autoimmune disease, of which the pathogens is remains obscure. Viral infection, particularly Epstein Barr viru (EBV) infection, has been considered a common pathogenic factor. This study suggests that c-Maf may be an important target in T cell differentiation during SLE progression, providing a potentially new perspective on the role of viral infection in the pathogenesis of autoimmune diseases.
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.
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.
摘要：
目的：系统性红斑狼疮（SLE）是一种多器官自身免疫性疾病，其中的病原体仍然是模糊的。病毒感染,特别是爱泼斯坦巴尔病毒（EBV）感染，已被认为是一种常见的致病因素。这项研究表明，c-Maf可能是SLE进展过程中T细胞分化的重要靶标，为病毒感染在自身免疫性疾病发病机制中的作用提供了一个潜在的新视角。
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。
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。
