BCL6公司
白细胞介素21
T细胞
生物
状态4
免疫学
CD40
染色质免疫沉淀
细胞分化
细胞生物学
细胞毒性T细胞
信号转导
车站3
B细胞
基因表达
免疫系统
抗体
基因
生发中心
斯达
遗传学
发起人
体外
作者
Suying Liu,Yanlei Yang,Liuting Zeng,Li Wang,Chengmei He,Zhilei Chen,Jinlei Sun,Taibiao Lyu,Mu Wang,Hua Chen,Fengchun Zhang
出处
期刊:Rheumatology
[Oxford University Press]
日期:2022-06-17
卷期号:62 (2): 946-957
被引量:13
标识
DOI:10.1093/rheumatology/keac304
摘要
Our data suggest that TOX in pSS naive CD4+ T cells is upregulated, which facilitates Tfh cell differentiation. Mechanistically, IFN-α induces TOX overexpression in naive CD4+ T cells through JAK-STAT1 signalling and TOX regulates BCL6 expression. Therefore, IFN-α-JAK-STAT1 signalling and TOX might be potential therapeutic targets in pSS.
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