Functional signaling of membrane-bound TL1A induces IFN-γ expression

被引：26

作者：

Biener-Ramanujan, Eva

Gonsky, Rivkah

Ko, Brian

Targan, Stephan R. ^{[1
]}

机构：

[1] Cedars Sinai Med Ctr, Ctr Inflammatory Bowel Dis, Los Angeles, CA 90048 USA

来源：

FEBS LETTERS | 2010年 / 584卷 / 11期

关键词：

TL1A signaling; Membrane-bound TL1A; Death domain receptor 3; IFN-gamma; HYPOHIDROTIC ECTODERMAL DYSPLASIA; INFLAMMATORY-BOWEL-DISEASE; NECROSIS-FACTOR FAMILY; RHEUMATOID-ARTHRITIS; T-CELL; ECTODYSPLASIN-A; RECEPTOR DR3; TNF; COSTIMULATOR; CYTOKINE;

D O I：

10.1016/j.febslet.2010.04.030

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

TL1A, a TNF member implicated in autoimmune diseases, is a transmembrane protein that is processed to release soluble TL1A (TL1A-S). TL1A-S induces a Th1 response, although the functional significance of membrane-bound TL1A (TL1A-M) remains unknown. We generated TL1A-M expression in HEK-293 cells capable of binding DR3-Fc. Co-incubating IL-12/IL-18-primed CD4(+)T cells with HEK-293 cells expressing TL1A-M induced 3-fold increase in IFN-gamma that was blocked by anti-TL1A Ab. These results demonstrate that TL1A-M can bind death domain receptor 3 (DR3) through cell-cell contact to induce downstream IFN-gamma secretion enhancement. Anti-TL1A antibodies designed to treat immune diseases should be verified to block both endogenous TL1A forms. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.

引用

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页码：2376 / 2380

页数：5

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