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:Therapeutic exploitation of neutrophils to fight cancer.
Therapeutic exploitation of neutrophils to fight cancer.
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基于抗体的免疫治疗是癌症治疗中一种有前景的策略。抗体可以直接抑制肿瘤生长,诱导补体依赖性细胞毒性,并诱导Fc受体介导的巨噬细胞和NK 细胞对肿瘤细胞的清除。然而,迄今为止,中性粒细胞作为潜在效应细胞在很大程度上被忽视,尽管它们是循环中最丰富的免疫细胞类型。中性粒细胞表现出异质性,尤其是在癌症背景下。因此,它们在癌症中的作用存在争议。尽管如此,中性粒细胞具有天然的抗肿瘤特性,适当的刺激,即通过抗体治疗进行特异性靶向,可诱导强效的肿瘤细胞杀伤,尤其是通过靶向免疫球蛋白A Fc受体(FcαRI,CD89)。在这篇综述中,我们探讨了中性粒细胞杀伤肿瘤细胞的机制以及中性粒细胞在诱导抗肿瘤免疫中的作用。此外,还讨论了治疗靶向的可能性。
Antibody-based immunotherapy is a promising strategy in cancer treatment. Antibodies can directly inhibit tumor growth, induce complement-dependent cytotoxicity and induce Fc receptor-mediated elimination of tumor cells by macrophages and natural killer cells. Until now, however, neutrophils have been largely overlooked as potential effector cells, even though they are the most abundant type of immune cells in the circulation. Neutrophils display heterogeneity, especially in the context of cancer.
Therefore, their role in cancer is debated. Nevertheless, neutrophils possess natural anti-tumor properties and appropriate stimulation, i. e. specific targeting via antibody therapy, induces potent tumor cell killing, especially via targeting of the immunoglobulin A Fc receptor (FcαRI, CD89). In this review we address the mechanisms of tumor cell killing by neutrophils and the role of neutrophils in induction of anti-tumor immunity.
Moreover, possibilities for therapeutic targeting are discussed.
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