Tumor derived cell-free nucleic acid upregulates programmed death-ligand 1 expression in neutrophil via intracellular Toll-like receptor signaling  

作　　者：Suguru Saito Duo-Yao Cao Tomohiro Shibata Yan Liu Aoi Otagiri-Hoshi Xiaojiang Cui Kenneth E.Bernstein 

机构地区：[1]Department of Biomedical Sciences,Cedars-Sinai Medical Center,Los Angeles,California,USA [2]Department of Pharmacology,School of Medicine,Yokohama City Univeristy,Yokohama,Kanagawa,Japan [3]Department of Surgery,Cedars-Sinai Medical Center,Los Angeles,California,USA [4]Graduate School of Comprehensive Human Science,University of Tsukuba,Tsukuba,Ibaraki,Japan [5]Department of Pathology and Laboratory Medicine,Cedars-Sinai Medical Center,Los Angeles,California,USA

出　　处：《Cancer Communications》2025年第1期4-8,共5页癌症通讯(英文)

基　　金：supported by the National Institutes of Health grants(R01AI164519,2R01CA151610,R21CA280458);American Heart Association’s Career Development award(23CDA1052548);U.S.Department of Defense(W81XWH-18-1-0067)and the Glazer Foundation.

摘　　要：Neutrophils are innate immune cells that function predominantly against pathogens,while recent studies have revealed additional crucial roles in various diseases,including cancers[1–3].For instance,neutrophils expressing the co-inhibitory molecule programmed death-ligand 1(PD-L1)were identified as novel immunosuppressive myeloid cells that impair cytotoxic T cell(CTL)activity via programmed cell death protein 1(PD-1)/PD-L1 interaction[4,5].Although some stimuli have been identified,it is still unclear whether the nucleic acid sensing system(NAS)participates in PD-L1 upregulation in neutrophils[6].Here,we report that increased cell-free nucleic acid(CFNA)upregulates PD-L1 expression via intracellular Toll-like receptor(TLR)activation in neutrophils following tumor expansion.

关 键 词：DEATH diseases programmed 

分 类 号：R73[医药卫生—肿瘤]