Hajizadeh Farnaz, Masjedi Ali, Heydarzedeh Asl Sima, Karoon Kiani Fariba, Peydaveisi Makwan, Ghalamfarsa Ghasem, Jadidi-Niaragh Farhad, Sevbitov Andrey
Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran.
Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Int Immunopharmacol. 2020 Oct;87:106853. doi: 10.1016/j.intimp.2020.106853. Epub 2020 Aug 2.
CD39 (nucleoside triphosphate diphosphohydrolase) and Ecto-5-nucleotidase (CD73) have been recognized as important factors mediating various pathological and physiological responses in the tumor microenvironment. Elevated expression of CD73 and CD39 is correlated with the over-production of adenosine in the tumor region. This increase is associated with an immunosuppressive state in the tumor site that enhances various tumor hallmarks such as metastasis, angiogenesis, and cell proliferation. Adenosine promotes these behaviors through interaction with four adenosine receptors, including A3R, A2BR, A2AR, and A1R. Signaling of these receptors reduces the function of immune effector cells and enhances the expansion and function of tumor-associated immune cells. Several studies have been shown the important role of adenosine/CD73/CD39/ARs axis in the immunopathogenesis of colorectal cancer. These findings imply that components of this axis can be considered as a worthy target for colorectal cancer immunotherapy. In this review, we summarized the role of CD73/CD39/adenosine/ARs in the immunopathogenesis of colorectal cancer.
CD39（核苷三磷酸二磷酸水解酶）和胞外5'-核苷酸酶（CD73）已被公认为介导肿瘤微环境中各种病理和生理反应的重要因素。CD73和CD39的表达升高与肿瘤区域腺苷的过量产生相关。这种增加与肿瘤部位的免疫抑制状态有关，该状态增强了转移、血管生成和细胞增殖等各种肿瘤特征。腺苷通过与包括A3R、A2BR、A2AR和A1R在内的四种腺苷受体相互作用来促进这些行为。这些受体的信号传导降低了免疫效应细胞的功能，并增强了肿瘤相关免疫细胞的扩增和功能。多项研究表明腺苷/CD73/CD39/ARs轴在结直肠癌免疫发病机制中的重要作用。这些发现意味着该轴的组成部分可被视为结直肠癌免疫治疗的一个有价值的靶点。在本综述中，我们总结了CD73/CD39/腺苷/ARs在结直肠癌免疫发病机制中的作用。
