炎症
白细胞介素17
T细胞
免疫学
促炎细胞因子
细胞因子
溃疡性结肠炎
T细胞受体
癌症研究
分泌物
细胞生物学
免疫系统
化学
医学
生物
内分泌学
内科学
疾病
作者
Q Fan,Wenjie Dai,Mechou Li,Tiantong Wang,Xinran Li,Zhaobin Deng,Wenzhe Li,Ming Li
标识
DOI:10.1016/j.intimp.2023.111130
摘要
Ulcerative colitis (UC) is a chronic, relapsing inflammatory disease that affects human intestines. Immune imbalance is one of the important factors inducing UC. After the activation of CD4+ T cells, pro-inflammatory cytokines are produced to induce colonic inflammation. α2,6-Sialylation, catalyzed by α2,6-sialyltransferase (ST6GAL1), affects the proliferation, activation, and T cell receptor (TCR) signaling of CD4+ T cells, but its role in CD4+ T cell polarization, regulation of Th17 / Treg balance, and its role in UC are still unclear. We found the number of CD4+ T and Th17 cells increased in colonic tissue with UC. The level of α2,6-sialylation of CD4+ T cells in patients with UC was significantly increased. De-α2,6-sialylation significantly reduced the symptoms of UC in rats. ST6GAL1 gene knockout inhibited the polarization of CD4+ T cells to Th17 cells, and promoted the polarization of CD4+ T cells to Treg cells. ST6GAL1 knockout significantly inhibited the IL-17 signaling pathway in CD4+ T cells and inhibited the secretion of pro-inflammatory cytokine IL-17a. ST6GAL1 and IL-17a are highly expressed in patients with UC, and there is a positive correlation between them. In conclusion, reduced α2,6-sialylation inhibits the polarization of CD4+ T cells to Th17 cells, inhibits IL-17a signaling pathway and reduces the level of pro-inflammatory cytokine IL-17a to alleviate the symptoms of UC, which is a potential novel target for the clinical treatment of UC.
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