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:Myeloid-Derived Suppressor Cells: Orchestrators of Tumor Immune Evasion and Therapeutic Vulnerabilities.
Myeloid-Derived Suppressor Cells: Orchestrators of Tumor Immune Evasion and Therapeutic Vulnerabilities.
分数与星级只用于站内排序 —— 不代表疗效、安全性或个人适用性。
髓源性抑制细胞(MDSC)具有异常表型、高度异质性和免疫抑制功能,是肿瘤免疫微环境的重要组成部分。MDSC通过抑制T细胞、B细胞、NK细胞和树突状细胞,同时促进调节性T细胞、肿瘤相关巨噬细胞和Th17细胞,推动癌症进展。除免疫抑制外,MDSC还促进肿瘤血管生成、肿瘤细胞干性、上皮-间质转化和转移前生态位形成。目前靶向MDSC的治疗策略包括清除MDSC、抑制其功能、诱导其分化,以及阻断MDSC募集和活化。多类治疗药物——包括化疗药物、单克隆抗体、小分子抑制剂和天然化合物——已显示出调节MDSC活性的效果。将靶向MDSC的治疗与免疫检查点抑制剂等现有免疫疗法联用,可能进一步改善抗肿瘤应答。
Myeloid-derived suppressor cells (MDSCs) are characterized by abnormal phenotypes, high heterogeneity, and immunosuppressive function. MDSCs are critical components in the tumor immune microenvironment, contributing to cancer progression by inhibiting T cells, B cells, NK cells, and dendritic cells while promoting regulatory T cells, tumor-associated macrophages, and Th17 cells. Beyond immunosuppression, MDSCs facilitate tumor angiogenesis, tumor cell stemness, epithelial-mesenchymal transition, and premetastatic niche formation.
Current therapeutic strategies targeting MDSCs include depletion, functional inhibition, induction of differentiation, and disruption of MDSC recruitment and activation. Various therapeutic agents-including chemotherapeutics, mAbs, small-molecule inhibitors, and natural compounds-have shown efficacy in modulating MDSC activity. Combining MDSC-targeted therapy with existing immunotherapies, such as immune checkpoint inhibitors, may further improve antitumor responses.
MEMBER ACCOUNT
登录成功会直接打开下一页。