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
采用武装型恒定 NK 细胞策略实现「多次射门」
英文原题：Taking "Multiple Shots on Goal" with an Armed Invariant NK Cell Approach.
查看英文原题
Taking "Multiple Shots on Goal" with an Armed Invariant NK Cell Approach.
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中文摘要
过继T细胞疗法对实体瘤的疗效有限，因此需要新的治疗方法。本期中，Chantzoura及其同事介绍了MiNK-215：一种新型异体成纤维细胞活化蛋白靶向嵌合抗原受体不变型NKT细胞疗法，并经工程化改造以分泌IL-15。研究显示，该疗法可通过清除成纤维细胞活化蛋白阳性的癌相关成纤维细胞并激活多种免疫细胞类型，重塑肿瘤微环境、增强抗肿瘤免疫。在小鼠肺肿瘤和人源类器官模型中，MiNK-215可促进持久、抗原特异性的T细胞应答，并克服免疫治疗耐药，且未造成脱靶毒性。相关研究见Chantzoura等人发表于第243页的文章。
展开英文摘要原文
Adoptive T-cell therapies have shown limited efficacy against solid tumors, so new approaches are required. In this issue, Chantzoura and colleagues describe MiNK-215, a novel allogeneic fibroblast activation protein-targeting chimeric antigen receptor invariant NK T-cell therapy engineered to secrete IL15.
They show that it can remodel the tumor microenvironment and enhance antitumor immunity by depleting fibroblast activation protein-positive cancer-associated fibroblasts and activating multiple immune cell types. In mouse lung tumor and human organoid models, MiNK-215 promotes durable, antigen-specific T-cell responses and overcomes resistance to immunotherapy without causing off-target toxicity. See related article by Chantzoura et al. , p. 243.
论文信息
- 作者
- Albelda SM
- 单位
- Division of Pulmonary and Critical Care Medicine, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.United States
- 文献类型
- 评论
- 期刊
- Cancer immunology research2026 Feb 3
- 原文标识
- PubMed 41528110 · DOI 10.1158/2326-6066.CIR-25-1344