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:Immune checkpoint TIM-3 in tumor immunotherapy.
Immune checkpoint TIM-3 in tumor immunotherapy.
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在过去十年中,免疫治疗已成为癌症治疗中的关键治疗策略。免疫检查点抑制剂(ICIs),如CTLA-4和PD-1单克隆抗体,已在不同类型的癌症中展现出显著的临床疗效。然而,免疫检查点疗法的总体成功率仍然较低。探索替代性免疫检查点分子势在必行。T细胞免疫球蛋白和含黏蛋白分子-3(TIM-3)表达于T细胞、自然杀伤(NK)细胞、巨噬细胞和树突状细胞,已被认为是有前景的肿瘤免疫治疗候选靶点。靶向TIM-3代表了癌症免疫治疗的一种有前景的方法,特别是通过合理设计与其他ICIs的新型联合疗法。在本综述中,我们全面总结了关于TIM-3在不同细胞类型中调控免疫应答作用的研究进展,并探讨了靶向TIM-3以实现更有效免疫治疗突破的理论框架。
Over the past decade, immunotherapy has emerged as a pivotal therapeutic strategy in cancer treatment. Immune checkpoint inhibitors (ICIs), such as CTLA-4 and PD-1 monoclonal antibodies, have demonstrated remarkable clinical efficacy in different types of cancer.
However, the overall success rate of immune checkpoint therapies remains low. Investigating alternative immune checkpoint molecules is imperative. T-cell immunoglobulin and mucin-containing molecule-3 (TIM-3), which is expressed in T cells, natural killer (NK) cells, macrophages, and dendritic cells, has gained recognition as a promising candidate for tumor immunotherapy.
Targeting TIM-3 represents a promising approach for cancer immunotherapy, particularly through the rational design of novel combination therapies with other ICIs. In this review, we present a comprehensive summary of the research advancements concerning the role of TIM-3 in regulating immune responses in different cell types and explore theoretical frameworks for targeting TIM-3 to achieve more effective immunotherapeutic breakthroughs.
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