炎症
细胞因子信号抑制因子1
肾小球肾炎
细胞因子
医学
信号转导
癌症研究
抑制器
免疫学
SOCS3
生物
细胞生物学
肾
内科学
癌症
作者
Jiuxu Bai,Lingling Wu,Xiaoniao Chen,Liqiang Wang,Qinggang Li,Yingjie Zhang,Jie Wu,Guangyan Cai,Xiangmei Chen
标识
DOI:10.3389/fimmu.2018.01982
摘要
Mesangial proliferative glomerulonephritis (MsGN) is a significant global threat to public health. Inflammation plays a crucial role in MsGN; however, the underlying mechanism remains unknown. Herein, we demonstrate that suppression of the cytokine signaling-1 (SOCS1)/signal transducer and activator of transcription 1 (STAT1) signaling pathway is associated with renal inflammation and renal injury in MsGN. Using MsGN rat (Thy1.1 GN) and mouse (Habu GN) models, renal SOCS1/STAT1 was determined to be associated with CD4+ T cell infiltration and related cytokines. In vitro, SOCS1 overexpression repressed IFN-γ-induced MHC class II and cytokine levels and STAT1 phosphorylation in mesangial cells. SOCS1 and STAT1 inhibitors significantly inhibited IFN-γ-induced CIITA promoter activity and MHC class II expression. In conclusion, our study emphasizes the pivotal role of the SOCS1/STAT1 axis in the regulation of inflammation in MsGN.
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