Cancer Immunology Program, Trescowthick Laboratories, Peter MacCallum Cancer Centre, St. Andrews Place, East Melbourne, Victoria 3002, Australia.
Trends Immunol. 2012 May;33(5):231-7. doi: 10.1016/j.it.2012.02.009. Epub 2012 Apr 7.
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.
肿瘤利用多种策略来逃避免疫监视。其中一种机制是在肿瘤微环境中产生腺苷，它强烈抑制抗肿瘤 T 细胞反应。肿瘤内的腺苷是由 CD73 产生的，CD73 是一种膜结合核苷酸酶，由肿瘤细胞、抑制性免疫亚群（如调节性 T 细胞[Tregs]和髓系来源的抑制细胞）和内皮细胞表达。最近的证据表明，靶向抑制 CD73 有可能减少肿瘤发生和转移，并增强 T 细胞导向治疗的效力。本综述概述了腺苷对抑制抗肿瘤反应的影响，以及支持在癌症治疗中靶向 CD73 的原理的证据。
