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PGE2 ameliorated viral myocarditis development and promoted IL-10-producing regulatory B cell expansion via MAPKs/AKT-AP1 axis or AhR signaling.
Cellular Immunology ( IF 4.3 ) Pub Date : 2019-12-06 , DOI: 10.1016/j.cellimm.2019.104025
Rong Chen 1 , Yuwen Cao 2 , Yu Tian 2 , Yufeng Gu 2 , Hongxiang Lu 1 , Shiqing Zhang 2 , Huaxi Xu 2 , Zhaoliang Su 1
Affiliation  

B10 cells, a specific subset of regulatory B cells, are capable of regulating immune response and restricting inflammation and autoimmune disease progression by producing IL-10. B10 cells frequently change significantly during inflammation and autoimmunity. However, how B10 cell populations change in viral myocarditis (VMC) remains unclear. Therefore, this work was conducted to clarify the changes in B10 cells and their potential mechanisms. Our results showed that the B10 cell frequency significantly changed in the VMC model. Changes in prostaglandin E2 (PGE2) levels in VMC model hearts were consistent with B10 expansion. PGE2 induced B10 cell expansion via the MAPKs/AKT-AP1 axis or AhR signaling. Additionally, PGE2-pretreated B10 cells inhibited naïve CD4+ T cell differentiation into Th17 cells. In vivo, PGE2 treatment or adoptive B10 cell transfer significantly restricted VMC development. Our results provide sufficient evidence that PGE2-induced B10 cell expansion may become a promising therapeutic approach for VMC and acute inflammatory injury.

中文翻译:

PGE2改善了病毒性心肌炎的发展,并通过MAPKs / AKT-AP1轴或AhR信号传导促进了IL-10产生的调节性B细胞扩增。

B10细胞是调节性B细胞的特定子集,能够通过产生IL-10来调节免疫反应并限制炎症和自身免疫疾病的进展。B10细胞在炎症和自身免疫过程中经常发生显着变化。但是,尚不清楚病毒心肌炎(VMC)中B10细胞的数量如何变化。因此,进行这项工作以阐明B10细胞的变化及其潜在机制。我们的结果表明,VMC模型中B10细胞的频率发生了显着变化。VMC模型心脏中前列腺素E2(PGE2)水平的变化与B10扩张一致。PGE2通过MAPKs / AKT-AP1轴或AhR信号传导诱导B10细胞扩增。此外,PGE2预处理的B10细胞抑制了幼稚的CD4 + T细胞分化为Th17细胞。体内,PGE2处理或过继B10细胞转移显着限制了VMC的发展。我们的结果提供了充分的证据,证明PGE2诱导的B10细胞扩增可能成为VMC和急性炎症损伤的有前途的治疗方法。
更新日期:2019-12-07
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