RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:DNAM-1 chimeric receptor-engineered NK cells: a new frontier for CAR-NK cell-based immunotherapy.
DNAM-1 chimeric receptor-engineered NK cells: a new frontier for CAR-NK cell-based immunotherapy.
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DNAM-1是主要的NK细胞活化受体,与NKG2D和NCRs一起,通过结合特定配体,强烈促进对肿瘤或病毒感染细胞的杀伤。DNAM-1特异性识别PVR和Nectin-2配体,这些配体表达于某些病毒感染细胞以及血液系统和实体恶性肿瘤的广谱肿瘤细胞上。迄今为止,虽然针对不同抗原嵌合受体(CARs)或嵌合NKG2D受体工程化的NK细胞已在临床前和临床研究中广泛测试,但使用DNAM-1嵌合受体工程化NK细胞仅在我们最近的概念验证研究中被提出,值得进一步开发。本展望研究的目的是描述使用这一新工具作为新型抗癌免疫疗法的理由。
DNAM-1 is a major NK cell activating receptor and, together with NKG2D and NCRs, by binding specific ligands, strongly contributes to mediating the killing of tumor or virus-infected cells. DNAM-1 specifically recognizes PVR and Nectin-2 ligands that are expressed on some virus-infected cells and on a broad spectrum of tumor cells of both hematological and solid malignancies.
So far, while NK cells engineered for different antigen chimeric receptors (CARs) or chimeric NKG2D receptor have been extensively tested in preclinical and clinical studies, the use of DNAM-1 chimeric receptor-engineered NK cells has been proposed only in our recent proof-of-concept study and deserves further development. The aim of this perspective study is to describe the rationale for using this novel tool as a new anti-cancer immunotherapy.
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