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本文引用的文献

1
Checkpoint blockade cancer immunotherapy targets tumour-specific mutant antigens.检查点阻断癌症免疫疗法靶向肿瘤特异性突变抗原。
Nature. 2014 Nov 27;515(7528):577-81. doi: 10.1038/nature13988.
2
Inhibition of CD39 enzymatic function at the surface of tumor cells alleviates their immunosuppressive activity.抑制肿瘤细胞表面的 CD39 酶活性可减轻其免疫抑制活性。
Cancer Immunol Res. 2015 Mar;3(3):254-65. doi: 10.1158/2326-6066.CIR-14-0018. Epub 2014 Nov 17.
3
Autophagy inhibition radiosensitizes in vitro, yet reduces radioresponses in vivo due to deficient immunogenic signalling.自噬抑制在体外具有放射增敏作用，但由于免疫原性信号不足，在体内降低了放射反应。
Cell Death Differ. 2014 Jan;21(1):92-9. doi: 10.1038/cdd.2013.124. Epub 2013 Sep 13.
4
Anticancer chemotherapy-induced intratumoral recruitment and differentiation of antigen-presenting cells.抗癌化疗诱导肿瘤内抗原呈递细胞的募集和分化。
Immunity. 2013 Apr 18;38(4):729-41. doi: 10.1016/j.immuni.2013.03.003. Epub 2013 Apr 4.
5
Stat3 and Gfi-1 transcription factors control Th17 cell immunosuppressive activity via the regulation of ectonucleotidase expression.Stat3 和 Gfi-1 转录因子通过调节细胞外核苷酸酶的表达来控制 Th17 细胞的免疫抑制活性。
Immunity. 2012 Mar 23;36(3):362-73. doi: 10.1016/j.immuni.2011.12.019. Epub 2012 Mar 8.
6
CD73-deficient mice are resistant to carcinogenesis.CD73 缺陷型小鼠对致癌作用有抵抗力。
Cancer Res. 2012 May 1;72(9):2190-6. doi: 10.1158/0008-5472.CAN-12-0420. Epub 2012 Mar 6.
7
Autophagy-dependent anticancer immune responses induced by chemotherapeutic agents in mice.化疗药物诱导小鼠依赖自噬的抗肿瘤免疫反应。
Science. 2011 Dec 16;334(6062):1573-7. doi: 10.1126/science.1208347.
8
Ectonucleotidases CD39 and CD73 on OvCA cells are potent adenosine-generating enzymes responsible for adenosine receptor 2A-dependent suppression of T cell function and NK cell cytotoxicity.卵巢癌细胞表面的外核苷酸酶 CD39 和 CD73 是产生腺苷的有效酶，可导致腺苷受体 2A 依赖性 T 细胞功能抑制和 NK 细胞细胞毒性。
Cancer Immunol Immunother. 2011 Oct;60(10):1405-18. doi: 10.1007/s00262-011-1040-4. Epub 2011 Jun 3.
9
Disordered purinergic signaling inhibits pathological angiogenesis in cd39/Entpd1-null mice.嘌呤能信号紊乱抑制CD39/Entpd1基因敲除小鼠的病理性血管生成。
Am J Pathol. 2007 Oct;171(4):1395-404. doi: 10.2353/ajpath.2007.070190. Epub 2007 Sep 6.
10
A2A adenosine receptor protects tumors from antitumor T cells.A2A 腺苷受体保护肿瘤免受抗肿瘤 T 细胞的攻击。
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CD39：作为免疫检查点的补充靶点以对抗肿瘤介导的免疫抑制。

CD39: A complementary target to immune checkpoints to counteract tumor-mediated immunosuppression.

作者信息

Bonnefoy Nathalie, Bastid Jérémy, Alberici Gilles, Bensussan Armand, Eliaou Jean-François

机构信息

IRCM, Institut de Recherche en Cancérologie de Montpellier , INSERM U1194, Université Montpellier , Montpellier, France.

OREGA Biotech ; Ecully, France.

出版信息

Oncoimmunology. 2015 Feb 3;4(5):e1003015. doi: 10.1080/2162402X.2014.1003015. eCollection 2015 May.

DOI:10.1080/2162402X.2014.1003015
PMID:26155397
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4485743/
Abstract

We report that CD39-expressing-melanoma cells inhibited both T-cell proliferation and the generation of cytotoxic effectors in an adenosine-dependent manner, and that treatment with a CD39-blocking antibody alleviated tumor-mediated immunosuppression. Thus, blocking CD39 ectonucleotidase may represent a novel immunotherapeutic strategy to restore antitumor immunity.

摘要

我们报告称，表达CD39的黑色素瘤细胞以腺苷依赖的方式抑制T细胞增殖和细胞毒性效应物的产生，并且用抗CD39阻断抗体治疗可减轻肿瘤介导的免疫抑制。因此，阻断CD39外核苷酸酶可能代表一种恢复抗肿瘤免疫力的新型免疫治疗策略。