CD73: A Novel Target for Cancer Immunotherapy

被引:190
作者
Zhang, Bin [1 ]
机构
[1] Univ Texas Hlth Sci Ctr San Antonio, Dept Med, Canc Therapy & Res Ctr, San Antonio, TX 78229 USA
关键词
T-CELLS; ADENOSINE RECEPTORS; TISSUE-DAMAGE; TUMOR-CELLS; PROTECTION; HYPOXIA; GENERATION; IMMUNITY;
D O I
10.1158/0008-5472.CAN-10-1544
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The promise of cancer immunotherapy has not been translated into clinical successes, in large part because of tumor-associated immune suppression that blocks effective antitumor immunity. Recent findings show a tumor-induced immunosuppressive mechanism, whereby tumor-derived CD73 functions as an ecto-enzyme to produce extracellular adenosine, which promotes tumor growth by limiting antitumor T-cell immunity via adenosine receptor signaling. Results with small molecule inhibitors, or monoclonal antibodies targeting CD73 in murine tumor models, suggest that targeted CD73 therapy is an important alternative and realistic approach to effective control of tumor growth. In particular, it helps T-cell-based therapy by enhancing the adaptive immune response machinery, which may increase the function of tumor-infiltrating T lymphocytes, and subsequently lead to improved survival in cancer patients. Cancer Res; 70(16); 6407-11. (C)2010 AACR.
引用
收藏
页码:6407 / 6411
页数:5
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