促炎细胞因子
细胞生物学
肿瘤坏死因子α
生物
受体
下调和上调
细胞凋亡
T细胞
细胞培养
Jurkat细胞
癌症研究
免疫系统
免疫学
炎症
生物化学
基因
遗传学
作者
Thi-Sau Migone,Jun Zhang,Xia Luo,Li Zhuang,Cecil Chen,Bugen Hu,June S. Hong,James W. Perry,Su-Fang Chen,Joe Zhou,Yun Hee Cho,Stephen J. Ullrich,Palanisamy Kanakaraj,Jeffrey A. Carrell,E Boyd,Henrik S. Olsen,Gang Hu,Laurie Pukac,Ding Liu,Jian Ni
出处
期刊:Immunity
[Cell Press]
日期:2002-03-01
卷期号:16 (3): 479-492
被引量:615
标识
DOI:10.1016/s1074-7613(02)00283-2
摘要
DR3 is a death domain-containing receptor that is upregulated during T cell activation and whose overexpression induces apoptosis and NF-kappaB activation in cell lines. Here we show that an endothelial cell-derived TNF-like factor, TL1A, is a ligand for DR3 and decoy receptor TR6/DcR3 and that its expression is inducible by TNF and IL-1alpha. TL1A induces NF-kappaB activation and apoptosis in DR3-expressing cell lines, while TR6-Fc protein antagonizes these signaling events. Interestingly, in T cells, TL1A acts as a costimulator that increases IL-2 responsiveness and secretion of proinflammatory cytokines both in vitro and in vivo. Our data suggest that interaction of TL1A with DR3 promotes T cell expansion during an immune response, whereas TR6 has an opposing effect.
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