Unlocking antitumor immunity with adenosine receptorblockers  

作　　者：Victoria A.Remley Joel Linden Todd W.Bauer Julien Dimastromatteo 

机构地区：[1]Department of Surgery,University of Virginia,Charlottesville,VA 22903,USA [2]Adovate,Charlottesville,VA 22901,USA [3]University of Virginia Comprehensive Cancer Center,Charlottesville,VA 22903,USA

出　　处：《Cancer Drug Resistance》2023年第4期748-767,共20页癌症耐药（英文）

摘　　要：Tumors survive by creating a tumor microenvironment(TME)that suppresses antitumor immunity.The TME suppresses the immune system by limiting antigen presentation,inhibiting lymphocyte and natural killer(NK)cell activation,and facilitating T cell exhaustion.Checkpoint inhibitors like anti-PD-1 and anti-CTLA4 are immunostimulatory antibodies,and their blockade extends the survival of some but not all cancer patients.Extracellular adenosine triphosphate(ATP)is abundant in inflamed tumors,and its metabolite,adenosine(ADO),is a driver of immunosuppression mediated by adenosine A2A receptors(A2AR)and adenosine A2B receptors(A2BR)found on tumor-associated lymphoid and myeloid cells.This review will focus on adenosine as a key checkpoint inhibitor-like immunosuppressive player in the TME and how reducing adenosine production or blocking A2AR and A2BR enhances antitumor immunity.

关 键 词：IMMUNOTHERAPY ADENOSINE adenosine receptors adenosine A2A receptors(A2AR) adenosine A2B receptors(A2BR) tumor cells immune cells tumor microenvironment 

分 类 号：R730.51[医药卫生—肿瘤]