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

收藏

页码：479 / 492

页数：14

相关论文

共 30 条

[11] Apo-3, a new member of the tumor necrosis factor receptor family, contains a death domain and activates apoptosis and NF-kappa B [J].

Marsters, SA ;

Sheridan, JP ;

Donahue, CJ ;

Pitti, RM ;

Gray, CL ;

Goddard, AD ;

Bauer, KD ;

Ashkenazi, A .

CURRENT BIOLOGY, 1996, 6 (12) :1669-1676

[12] Identification of a ligand for the death-domain-containing receptor Apo3 [J].

Marsters, SA ;

Sheridan, JP ;

Pitti, RM ;

Brush, J ;

Goddard, A ;

Ashkenazi, A .

CURRENT BIOLOGY, 1998, 8 (09) :525-528

[13] Effects of a dominant interfering mutant of FADD on signal transduction in activated T cells [J].

Newton, K ;

Kurts, C ;

Harris, AW ;

Strasser, A .

CURRENT BIOLOGY, 2001, 11 (04) :273-276

[14] Genomic amplification of a decoy receptor for Fas ligand in lung and colon cancer [J].

Pitti, RM ;

Marsters, SA ;

Lawrence, DA ;

Roy, M ;

Kischkel, FC ;

Dowd, P ;

Huang, A ;

Donahue, CJ ;

Sherwood, SW ;

Baldwin, DT ;

Godowski, PJ ;

Wood, WI ;

Gurney, AL ;

Hillan, KJ ;

Cohen, RL ;

Goddard, AD ;

Botstein, D ;

Ashkenazi, A .

NATURE, 1998, 396 (6712) :699-703

[15]

Schneider P, 1999, EUR J IMMUNOL, V29, P1785, DOI 10.1002/(SICI)1521-4141(199906)29:06<1785::AID-IMMU1785>3.0.CO

[16]

2-U

[17] LARD: A new lymphoid-specific death domain containing receptor regulated by alternative pre-mRNA splicing [J].

Screaton, GR ;

Xu, XN ;

Olsen, AL ;

Cowper, AE ;

Tan, RS ;

McMichael, AJ ;

Bell, JI .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (09) :4615-4619

[18] The multifaceted role of Fas signaling in immune cell homeostasis and autoimmunity [J].

Siegel, RM ;

Chan, FKM ;

Chun, HJ ;

Lenardo, MJ .

NATURE IMMUNOLOGY, 2000, 1 (06) :469-474

[19] Characterization of a novel TNF-like ligand and recently described TNF ligand and TNF receptor superfamily genes and their constitutive and inducible expression in hematopoietic and non-hematopoietic cells [J].

Tan, KB ;

Harrop, J ;

Reddy, M ;

Young, P ;

Terrett, J ;

Emery, J ;

Moore, G ;

Truneh, A .

GENE, 1997, 204 (1-2) :35-46

[20] Targeted disruption of the mouse Caspase 8 gene ablates cell death induction by the TNF receptors, Fas/Apo1, and DR3 and is lethal prenatally [J].

Varfolomeev, EE ;

Schuchmann, M ;

Luria, V ;

Chiannilkulchai, N ;

Beckmann, JS ;

Mett, IL ;

Rebrikov, D ;

Brodianski, VM ;

Kemper, OC ;

Kollet, O ;

Lapidot, T ;

Soffer, D ;

Sobe, T ;

Avraham, KB ;

Goncharov, T ;

Holtmann, H ;

Lonai, P ;

Wallach, D .

IMMUNITY, 1998, 9 (02) :267-276