Department of Immunology, Hebei Medical University, Shijiazhuang, Hebei, China; Key Laboratory of Immune mechanism and Intervention on Serious Disease in Hebei Province, Shijiazhuang, Hebei, China; Department of Rheumatology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
Department of Immunology, Hebei Medical University, Shijiazhuang, Hebei, China; Key Laboratory of Immune mechanism and Intervention on Serious Disease in Hebei Province, Shijiazhuang, Hebei, China.
Mol Immunol. 2024 Jul;171:22-35. doi: 10.1016/j.molimm.2024.05.003. Epub 2024 May 14.
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.
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.
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.
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.
系统性红斑狼疮（SLE）是一种多器官自身免疫性疾病，其病原体仍不清楚。病毒感染，特别是 EBV 感染，被认为是一个常见的致病因素。本研究表明，c-Maf 可能是 SLE 进展中 T 细胞分化的一个重要靶点，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。
通过 ELISA 测量 EBV 感染的 SLE 患者的细胞因子，并结合其临床数据进行评估。采用 FCM、WB、RT-PCR 等方法分析 SLE 患者和 MRL/LPR 小鼠中的 IFN-α、c-Maf 和 Th17/Treg 细胞的分化。在细胞和小鼠感染 EBV 或病毒模拟物 poly（dA:dT）后，研究上述指标的变化。通过 si-RNA 技术确定 IFN-α、STAT3、c-Maf 和 Th17 细胞之间的关系。
许多 SLE 患者并发病毒感染；进一步研究表明，病毒感染，特别是 EBV，参与 SLE 的发生。本研究表明，病毒感染可能通过 IFN-α 激活 STAT3 促进 IFN-α 的分泌，抑制 c-Maf 的表达，增加 Th17 细胞的分化，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。
本研究表明，EBV 感染可能通过 IFN-α 激活 STAT3、抑制 c-Maf、导致 Th17/Treg 免疫失衡，从而促进 SLE 的发生。我们的工作为 SLE 的发病机制和治疗提供了新的思路。
