TNF superfamily in inflammatory disease: translating basic insights

被引：180

作者：

Croft, Michael ^{[1
]}

Duan, Wei ^{[1
]}

Choi, Heonsik ^{[1
]}

Eun, So-Young ^{[1
]}

Madireddi, Shravan ^{[1
]}

Mehta, Amit ^{[1
]}

机构：

[1] La Jolla Inst Allergy & Immunol, Div Immune Regulat, La Jolla, CA 92037 USA

来源：

TRENDS IN IMMUNOLOGY | 2012年 / 33卷 / 03期

基金：

美国国家卫生研究院;

关键词：

SYSTEMIC-LUPUS-ERYTHEMATOSUS; COLLAGEN-INDUCED ARTHRITIS; RHEUMATOID-ARTHRITIS; AUTOIMMUNE-DISEASE; ENTRY MEDIATOR; INTESTINAL INFLAMMATION; IMMUNE-RESPONSE; DEFICIENT MICE; CELL-FUNCTION; ASSOCIATION;

D O I：

10.1016/j.it.2011.10.004

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

071005 [微生物学]; 100108 [医学免疫学];

摘要：

The tumor necrosis factor (TNF) and TNF receptor superfamilies (TNFSF and TNFRSF) consist of approximately 50 membrane and soluble proteins that can modulate cellular function. Most of these molecules are expressed by or can target cells of the immune system, and they have a wide range of actions including promoting cellular differentiation, survival, and production of inflammatory cytokines and chemokines. Emerging data show that TNFSF ligand receptor signaling pathways are active in inflammatory and autoimmune disease. Furthermore, several genetic polymorphisms in TNFSF and TNFRSF associate with susceptibility to developing disease. Here, we examine recent data regarding the potential of these molecules as targets for therapy of autoimmune and inflammatory disease.

引用

页码：144 / 152

页数：9

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