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:Protocol for evaluating antitumor activity of KIR3DL3 blockade in an NK cell-based xenogeneic lung tumor model.
Protocol for evaluating antitumor activity of KIR3DL3 blockade in an NK cell-based xenogeneic lung tumor model.
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人杀伤细胞免疫球蛋白样受体,三个Ig结构域和长胞质尾(KIR3DL3)表达于自然杀伤(NK)细胞,是新发现的B7家族成员HERV-H LTR关联蛋白2(HHLA2)的抑制性受体。在此,我们总结了KIR3DL3+人NK细胞的分离和扩增,以及内部抗KIR3DL3单克隆抗体(mAb)的体外功能表征。我们还描述了一种基于人NK细胞的异种肺肿瘤模型,用于在体内测试KIR3DL3阻断的治疗活性。关于本方案使用和执行的完整细节,请参阅Wei et al.(2021)。
Human killer cell immunoglobulin-like receptor, three Ig domains and long cytoplasmic tail (KIR3DL3) is expressed on natural killer (NK) cells and is a newly identified inhibitory receptor for B7 family member HERV-H LTR-associating protein 2 (HHLA2).
Here, we summarize the isolation and expansion of KIR3DL3 + human NK cells, and in vitro functional characterization of in-house anti-KIR3DL3 monoclonal antibody (mAb).
We also describe a human NK cell-based xenogeneic lung tumor model for testing the therapeutic activity of KIR3DL3 blockade in vivo . For complete details on the use and execution of this protocol, please refer to Wei et al. (2021).
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