Emerging Functions of Amphiregulin in Orchestrating Immunity, Inflammation, and Tissue Repair

被引：463

作者：

Zaiss, Dietmar M. W. ^{[1
]}

Gause, William C. ^{[2
]}

Osborne, Lisa C. ^{[3
]}

Artis, David ^{[3
]}

机构：

[1] Univ Edinburgh, Inst Immunol & Infect Res, Ashworth Labs, Edinburgh EH9 3FL, Midlothian, Scotland

[2] Rutgers State Univ, New Jersey Med Sch, Ctr Immun & Inflammat, Dept Med, Newark, NJ 07101 USA

[3] Cornell Univ, Jill Roberts Inst Res IBD, Joan & Sanford I Weill Dept Med, Dept Microbiol & Immunol,Weill Cornell Med Coll, New York, NY 10021 USA

来源：

IMMUNITY | 2015年 / 42卷 / 02期

基金：

英国医学研究理事会; 美国国家卫生研究院;

关键词：

GROWTH-FACTOR RECEPTOR; INNATE LYMPHOID-CELLS; REGULATORY T-CELLS; HUMAN MAST-CELLS; HEPARAN-SULFATE; GENE-EXPRESSION; TGF-BETA; AIRWAY HYPERREACTIVITY; SUSTAINED ACTIVATION; DENDRITIC CELLS;

D O I：

10.1016/j.immuni.2015.01.020

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Type 2 inflammatory responses can be elicited by diverse stimuli, including toxins, venoms, allergens, and infectious agents, and play critical roles in resistance and tolerance associated with infection, wound healing, tissue repair, and tumor development. Emerging data suggest that in addition to characteristic type 2-associated cytokines, the epidermal growth factor (EGF)-like molecule Amphiregulin (AREG) might be a critical component of type 2-mediated resistance and tolerance. Notably, numerous studies demonstrate that in addition to the established role of epithelial- and mesenchymal-derived AREG, multiple leukocyte populations including mast cells, basophils, group 2 innate lymphoid cells (ILC2s), and a subset of tissue-resident regulatory CD4(+) T cells can express AREG. In this review, we discuss recent advances in our understanding of the AREG-EGF receptor pathway and its involvement in infection and inflammation and propose a model for the function of this pathway in the context of resistance and tissue tolerance.

引用

页码：216 / 226

页数：11

共 112 条

[1] MODULATION OF THE RECEPTOR-BINDING AFFINITY OF AMPHIREGULIN BY MODIFICATION OF ITS CARBOXYL-TERMINAL TAIL [J].