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黑色素瘤中的代谢环境:CD73/腺苷介导的免疫抑制作用

The metabolic milieu in melanoma: Role of immune suppression by CD73/adenosine.

作者信息

Passarelli Anna, Tucci Marco, Mannavola Francesco, Felici Claudia, Silvestris Francesco

机构信息

Department of Biomedical Sciences and Human Oncology, University of Bari Aldo Moro, Bari, Italy.

出版信息

Tumour Biol. 2019 Apr;42(4):1010428319837138. doi: 10.1177/1010428319837138.

Abstract

The mechanisms leading to immune escape of melanoma have been largely investigated in relation to its tumour immunogenicity and features of inflamed microenvironment that promote the immune suppression during the disease progression. These findings have recently led to advantages in terms of immunotherapy-based approaches as rationale for overcoming the immune escape. However, besides immune checkpoints, other mechanisms including the adenosine produced by ectonucleotidases CD39 and CD73 contribute to the melanoma progression due to the immunosuppression induced by the tumour milieu. On the other hand, CD73 has recently emerged as both promising therapeutic target and unfavourable prognostic biomarker. Here, we review the major mechanisms of immune escape activated by the CD39/CD73/adenosine pathway in melanoma and focus potential therapeutic strategies based on the control of CD39/CD73 downstream adenosine receptor signalling. These evidences provide the basis for translational strategies of immune combination, while CD73 would serve as potential prognostic biomarker in metastatic melanoma.

摘要

黑色素瘤免疫逃逸的机制在很大程度上已根据其肿瘤免疫原性以及在疾病进展过程中促进免疫抑制的炎症微环境特征进行了研究。这些发现最近在基于免疫疗法的方法方面带来了优势,作为克服免疫逃逸的理论依据。然而,除了免疫检查点之外,包括外核苷酸酶CD39和CD73产生的腺苷在内的其他机制,由于肿瘤微环境诱导的免疫抑制,也促进了黑色素瘤的进展。另一方面,CD73最近已成为既有前景的治疗靶点,又有不良预后生物标志物。在这里,我们综述了黑色素瘤中由CD39/CD73/腺苷途径激活的免疫逃逸的主要机制,并重点介绍了基于控制CD39/CD73下游腺苷受体信号传导的潜在治疗策略。这些证据为免疫联合的转化策略提供了基础,而CD73将作为转移性黑色素瘤的潜在预后生物标志物。

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