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:Mechanisms of myeloid-derived suppressor cell-mediated immunosuppression in colorectal cancer and related therapies.
Mechanisms of myeloid-derived suppressor cell-mediated immunosuppression in colorectal cancer and related therapies.
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严重免疫抑制是结直肠癌(CRC)的一个标志。髓源性抑制细胞(MDSCs)是肿瘤基质中最丰富的成分之一,在CRC的侵袭、转移和免疫逃逸中发挥重要作用。MDSCs通过抑制免疫反应细胞(包括T细胞和NK 细胞)的增殖和活化,以及通过诱导免疫抑制细胞(如调节性T细胞和肿瘤相关巨噬细胞)的增殖,从而促进癌细胞的生长,形成免疫抑制微环境。因此,MDSCs是CRC中免疫抑制微环境出现的关键贡献者,并在抗肿瘤免疫崩溃中发挥重要作用。在这篇叙述性综述中,我们探讨了MDSCs促成免疫抑制微环境的机制、当前针对MDSCs的治疗方法和技术,以及调节MDSCs在CRC治疗中的治疗潜力。本研究为提高CRC患者的生存率提供了思路和方法。
Severe immunosuppression is a hallmark of colorectal cancer (CRC). Myeloid-derived suppressor cells (MDSCs), one of the most abundant components of the tumor stroma, play an important role in the invasion, metastasis, and immune escape of CRC.
MDSCs create an immunosuppressive microenvironment by inhibiting the proliferation and activation of immunoreactive cells, including T and natural killer cells, as well as by inducing the proliferation of immunosuppressive cells, such as regulatory T cells and tumor-associated macrophages, which, in turn, promote the growth of cancer cells.
Thus, MDSCs are key contributors to the emergence of an immunosuppressive microenvironment in CRC and play an important role in the breakdown of antitumor immunity. In this narrative review, we explore the mechanisms through which MDSCs contribute to the immunosuppressive microenvironment, the current therapeutic approaches and technologies targeting MDSCs, and the therapeutic potential of modulating MDSCs in CRC treatment.
This study provides ideas and methods to enhance survival rates in patients with CRC.
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