RNA 编辑酶 ADAR1 的缺失可增强 NK 细胞的抗肿瘤免疫
Depletion of the RNA-Editing Enzyme ADAR1 Invigorates the Antitumor Immunity of NK Cells.
功能性耗竭和低效的肿瘤浸润率限制了基于自然杀伤(NK)细胞的癌症免疫疗法的有效性。
ALL SOURCES
Depletion of the RNA-Editing Enzyme ADAR1 Invigorates the Antitumor Immunity of NK Cells.
功能性耗竭和低效的肿瘤浸润率限制了基于自然杀伤(NK)细胞的癌症免疫疗法的有效性。
Intraperitoneal infusion of NKG2D CAR-NK cells induces endogenous CD8(+) T cell activation in patients with advanced colorectal cancer.
9 例患者中有 3 例达到疾病稳定,疾病控制率为 33.3%。
LLT1 overexpression renders allogeneic-NK resistance and facilitates the generation of enhanced universal CAR-T cells.
根据这些结果,LLT1 过表达增强了 UCAR-T 细胞的活性并防止同种异体排斥反应,为通用型 CAR-T 细胞疗法的开发提供了重要见解。
Intratumoral CD38(+)CD19(+)B cells associate with poor clinical outcomes and immunosuppression in patients with pancreatic ductal adenocarcinoma.
我们发现调节性 B 细胞样 CD38⁺ B 细胞浸润是胰腺导管腺癌(PDAC)的独立预后因素。
CD38-Specific CAR Integrated into CD38 Locus Driven by Different Promoters Causes Distinct Antitumor Activities of T and NK Cells.
这些结果支持了 CD38 CAR-T/NK 对 T-ALL 的疗效,并证明“二合一”策略能够解决自相残杀问题并增强肿瘤清除,为临床转化铺平了道路。
Identification of potential resistance mechanisms and therapeutic targets for the relapse of BCMA CAR-T therapy in relapsed/refractory multiple myelom
我们比较了BCMA CAR-T治疗前和BCMA CAR-T治疗后复发时CD45 + BM细胞的异质性。
Regulation of CD38 on Multiple Myeloma and NK Cells by Monoclonal Antibodies.
CD38在多发性骨髓瘤(MM)细胞上高表达,并在调控肿瘤发生发展中发挥作用。
High PD-1 expression in pre-treatment peripheral lymphocytes associated with poor immune checkpoint inhibitor response in patients with recurrent or m
我们的结果表明,PBL 中 PD-1 高表达预示 RMHNSCC 患者接受抗 PD-1 ICI 治疗结局不佳。
Mass cytometric analysis of circulating immune landscape in primary central nervous system lymphoma.
PCNSL中的循环免疫景观以单核细胞激活偏斜、T细胞终末耗竭及化疗诱导的效应T细胞扩增为特征。我们的发现将外周免疫特征与肿瘤微环境生物学联系起来。理解这些系统性免疫改变可能为肿瘤免疫逃逸提供见解,并为逆转PCNSL相关免疫抑制提供路线图。
Reduced ALDH1A1 expression in multiple myeloma cells increases resistance to daratumumab via downregulation of retinoic acid.
多发性骨髓瘤(MM)在复发/难治性病例中仍具挑战性,原因是对蛋白酶体抑制剂或抗CD38抗体daratumumab(Dara)等疗法产生耐药性。
MEMBER ACCOUNT
登录成功会直接打开下一页。