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:Enhancing immunotherapy response in melanoma: myeloid-derived suppressor cells as a therapeutic target.
Enhancing immunotherapy response in melanoma: myeloid-derived suppressor cells as a therapeutic target.
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尽管免疫检查点抑制剂(ICIs)在黑色素瘤治疗中取得了显著成功,但对其耐药仍是重大的临床挑战。髓源性抑制细胞(MDSCs)代表了一类异质性髓系细胞群体,能够抑制由T细胞和NK 细胞介导的抗肿瘤免疫应答并促进肿瘤生长。它们是ICI耐药的主要因素,并在形成免疫抑制性肿瘤微环境中发挥关键作用。因此,靶向MDSCs被认为是提高ICIs治疗效果的有前景的策略。本综述阐述了MDSC介导免疫抑制的机制、针对MDSC的临床前和临床研究,以及抑制MDSC功能以改善黑色素瘤免疫治疗的潜在策略。
Despite the remarkable success of immune checkpoint inhibitors (ICIs) in melanoma treatment, resistance to them remains a substantial clinical challenge. Myeloid-derived suppressor cells (MDSCs) represent a heterogeneous population of myeloid cells that can suppress antitumor immune responses mediated by T and natural killer cells and promote tumor growth. They are major contributors to ICI resistance and play a crucial role in creating an immunosuppressive tumor microenvironment.
Therefore, targeting MDSCs is considered a promising strategy to improve the therapeutic efficacy of ICIs. This Review describes the mechanism of MDSC-mediated immune suppression, preclinical and clinical studies on MDSC targeting, and potential strategies for inhibiting MDSC functions to improve melanoma immunotherapy.
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