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IFN-α affects Th17/Treg cell balance through c-Maf and associated with the progression of EBV- SLE.
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- Author(s): Zhang, Yue1,2,3 (AUTHOR); Wang, Jiachao1,2 (AUTHOR); Fang, Yaqi1,2 (AUTHOR); Liang, Wenzhang1,2 (AUTHOR); Lei, Lingyan3 (AUTHOR); Wang, Junhai1,2 (AUTHOR); Gao, Xue1,2 (AUTHOR); Ma, Cuiqing1,2 (AUTHOR); Li, Miao1,2 (AUTHOR); Guo, Huifang1,3 (AUTHOR) ; Wei, Lin1,2 (AUTHOR)
- Source:
Molecular Immunology. Jul2024, Vol. 171, p22-35. 14p.- Subject Terms:
- Source:
- Additional Information
- Abstract: 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. • EBV participatede in SLE development through disrupting the Th17 / Treg immune balance. • EBV induces the production of IFN-α, which in turn affects the regulation of Th17/Treg cell differentiation by c-Maf. • EBV infections promote IFN-α secretion, suppresses c-Maf expression through STAT3 pathway. • At the same time, antiviral therapy will be very important for the treatment of SLE. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Molecular Immunology is the property of Pergamon Press - An Imprint of Elsevier Science and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
- Abstract:
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