CD73: a potent suppressor of antitumor immune responses

被引：300

作者：

Beavis, Paul. A. ^{[1
]}

Stagg, John ^{[2
,3
]}

Darcy, Phillip K. ^{[1
,4
]}

Smyth, Mark J. ^{[1
,4
]}

机构：

[1] Peter MacCallum Canc Ctr, Canc Immunol Program, Trescowthick Labs, Melbourne, Vic 3002, Australia

[2] Univ Montreal, Inst Canc Montreal, Montreal, PQ H2L 4M1, Canada

[3] Ctr Hosp Univ Montreal, Ctr Rech, Fac Pharm, Montreal, PQ H2L 4M1, Canada

[4] Univ Melbourne, Sir Peter MacCallum Dept Oncol, Melbourne, Vic 3010, Australia

来源：

TRENDS IN IMMUNOLOGY | 2012年 / 33卷 / 05期

基金：

英国医学研究理事会;

关键词：

CD73; adenosine; cancer; immunity; REGULATORY T-CELLS; A2A ADENOSINE RECEPTOR; EXTRACELLULAR ADENOSINE; TUMOR-GROWTH; ECTO-5'-NUCLEOTIDASE ACTIVITY; CYTOKINE PRODUCTION; ADAPTIVE IMMUNITY; HUMAN-LYMPHOCYTES; ATP RELEASE; EXPRESSION;

D O I：

10.1016/j.it.2012.02.009

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Tumors use several strategies to evade immunosurveillance. One such mechanism is the generation of adenosine within the tumor microenvironment, which potently suppresses antitumor T cell responses. Adenosine within the tumor is generated by CD73, a membrane-bound nucleotidase that is expressed by tumor cells, suppressive immune subsets such as T regulatory cells (Tregs) and myeloid-derived suppressor cells and endothelial cells. Recent evidence suggests that targeted inhibition of CD73 has the potential to reduce tumorigenesis and metastasis, as well as enhancing the potency of T-cell-directed therapies. This review outlines the impact of adenosine on suppressing the antitumor response and the evidence supporting the rationale for CD73 targeting in the treatment of cancer.

引用

页码：231 / 237

页数：7

共 84 条

[1] CD73 engagement promotes lymphocyte binding to endothelial cells via a lymphocyte function-associated antigen-1-dependent mechanism [J].