进一步分析发现CD58的缺失会一直与T细胞CD2的链接,减少T细胞的激活、抑制肿瘤T细胞浸润以及细胞增殖,同时增加PDL1蛋白来促进免疫逃逸。 为了进一步明确相关机制,作者通过CRISPR-Cas9以及蛋白质组学筛选,确认了CMTM6对于CD58缺失介导的PDL1上调至关重要。CD58和PDL1对于CMTM6结合的竞争确定了他们主要通过内体循环还是通过溶...
肿瘤免疫微环境目的:明确CMTM6以及PD-L1/CD4/CD8在肝癌中的表达及其与肝癌患者临床病理特征的关系,阐明CMTM6表达,CMTM6/PDL1共表达及其联合T细胞浸润对肝癌患者生存预后的影响;探讨CMTM6异常表达对肝癌细胞增殖,凋亡,周期,侵袭和迁移等生物学功能的影响;筛选并验证CMTM6参与调控的免疫相关信号通路,靶基因及免疫浸润...
[37] XIA X,LI R,ZHOU P,et al.Decreased NSG3 enhances PD- L1 expression by Erk1/2 pathway to promote pancreatic cancer progress[J].Am J Cancer Res,2021,11(3):916-929. [38] BIRNBAUM D J,FINETTI P,LOPRESTI A,et al.Prognostic value of PDL1 expression in pancreatic cancer[J].Onco...
CMTM6 has been mostly studied in the context of anti-tumor immunity by regulating plasma membrane expression of programmed death ligand-1 (PDL1/CD274)10. However, no change in either expression or localization of PDL1 was observed in conditional CMTM6 KO mice suggesting that CMTM6 regulates axo...
CMTM6 has been mostly studied in the context of anti-tumor immunity by regulating plasma membrane expression of programmed death ligand-1 (PDL1/CD274)10. However, no change in either expression or localization of PDL1 was observed in conditional CMTM6 KO mice suggesting that CMTM6 regulates ...
Expression of CMTM6 was reported to limit anti-tumor immunity29,30 via regulating abundance and localization of programmed death ligand-1 (PDL1/CD274) at the surface of cancer cells, at least in vitro. However, we did not find evidence of CMTM6 influencing CD274 in Schwann cells, at least...
2019 年 8 月 30 日,DakoNorthAmerica(代理人:安捷 伦科技(中国)有限公司)的 PD-L1 免疫组织化学法检测试剂盒 PDL1IHC22C3pharmDx(下简称“DAKO22C3”)正式获得国家药品监督管理局(NMPA)批 准上市,可辅助鉴别可使用帕博利珠单抗治疗的非小细胞肺癌患者,成为国内获批的 首个 PD-L1 检测试剂盒。2020 年 5 ...
肺腺癌作为非小细胞肺癌重要类型，致死率高，疾病进展迅速，严重威胁人类健康[1-3]。肺腺癌一半以上的患者被诊断为无法治愈的局部晚期或转移性疾病。近年来，免疫治疗在肺癌中取得重大进展,其中，靶向PD1-PDL1途径成为治疗非小细胞肺癌的研究热点。如今，免疫相关药物已被批准并应用于临床，例如PD-1抑制剂（nivolumab和...
用于恶性肿瘤的治疗方案选择,疗效和预后,恶性肿瘤主要包括黑色素瘤,非小细胞肺癌,膀胱癌,肾癌,胃癌,结直肠癌,前列腺癌,宫颈癌,乳腺癌等.本发明为制备用于免疫治疗恶性肿瘤的抗体药物提供基础,所用抗体药物可为人源化后的CMTM6单抗全长或部分片段(Fab,F(ab)'2或ScFv),或将人源化后的CMTM6单抗与PDL1单抗联合...
Cancer Cell | CD58(LFA-3)缺失通过促进CMTM6上调PDL1抑制抗肿瘤免疫 这项研究还是聚焦在肿瘤免疫,分析在免疫检查点治疗中出现抵抗的原因及其机制。过往研究发现在肿瘤细胞中往往会自主降低CD58的表达,而这常与ICB治疗抵抗以及T细胞耗竭相关。但是机制并不清楚。