TL1A is a TNF-like ligand and functions as a T cell for DR3 and TR6/DcR3 costimulator

被引：524

作者：

Migone, TS ^{[1
]}

Zhang, J ^{[1
]}

Luo, X ^{[1
]}

Zhuang, L ^{[1
]}

Chen, C ^{[1
]}

Hu, BG ^{[1
]}

Hong, JS ^{[1
]}

Perry, JW ^{[1
]}

Chen, SF ^{[1
]}

Zhou, JXH ^{[1
]}

Cho, YH ^{[1
]}

Ullrich, S ^{[1
]}

Kanakaraj, P ^{[1
]}

Carrell, J ^{[1
]}

Boyd, E ^{[1
]}

Olsen, HS ^{[1
]}

Hu, G ^{[1
]}

Pukac, L ^{[1
]}

Liu, D ^{[1
]}

Ni, J ^{[1
]}

Kim, S ^{[1
]}

Gentz, R ^{[1
]}

Feng, P ^{[1
]}

Moore, PA ^{[1
]}

Ruben, SM ^{[1
]}

Wei, P ^{[1
]}

机构：

[1] Human Genome Sci Inc, Rockville, MD 20850 USA

来源：

IMMUNITY | 2002年 / 16卷 / 03期

关键词：

D O I：

10.1016/S1074-7613(02)00283-2

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

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.

引用

页码：479 / 492

页数：14

共 30 条

[1] Apoptosis control by death and decoy receptors [J].