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:T-cell immunoglobulin and ITIM domain in cancer immunotherapy: A focus on tumor-infiltrating regulatory T cells.
T-cell immunoglobulin and ITIM domain in cancer immunotherapy: A focus on tumor-infiltrating regulatory T cells.
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T细胞免疫球蛋白和ITIM结构域(TIGIT)是一种新型免疫检查点。重要的是,免疫检查点分子通过多种抗肿瘤抑制机制促进癌症进展。TIGIT是一种表达于T细胞、NK 细胞和调节性T细胞上的抑制性受体,近年来作为癌症免疫治疗的主要新兴靶点而受到关注。调节性T细胞(Tregs)在免疫稳态中发挥关键作用。具体而言,肿瘤浸润性Tregs通过限制抗肿瘤免疫和支持肿瘤免疫逃逸来促进癌症进展。在这篇综述中,我们总结了目前对TIGIT和肿瘤浸润性Tregs的认识。在此,我们回顾了在理解导致肿瘤浸润性Tregs丰度的机制方面的最新进展,以优化Tregs靶向治疗。总体而言,靶向Tregs的抗TIGIT疗法在强效癌症靶向治疗方面具有巨大前景。
T-cell immunoglobulin and ITIM domain (TIGIT) is a novel type of immune checkpoint.
Importantly, immune checkpoint molecules promote cancer progression by various antitumor suppressive mechanisms. TIGIT is an inhibitory receptor expressed on T cells, natural killer cells, and regulatory T cells that was recently attracted attention as a major emerging target for cancer immunotherapy.
Regulatory T cells (Tregs) play crucial roles in immune homeostasis. Specifically, tumor-infiltrating Tregs promote cancer progression by restricting antitumor immunity and supporting tumor immune escape. In this review, we summarized the current understanding on TIGIT and tumor-infiltrating Tregs.
Here, we reviewed the latest advances in the understanding of mechanisms causing tumor-infiltrating Tregs abundance to optimize Tregs targeted therapy. Collectively, anti-TIGIT targeting Tregs hold great promise for potent cancer target therapy.
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