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:Target therapy of TIGIT; a novel approach of immunotherapy for the treatment of colorectal cancer.
Target therapy of TIGIT; a novel approach of immunotherapy for the treatment of colorectal cancer.
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T细胞免疫球蛋白和免疫受体酪氨酸抑制基序结构域(TIGIT)是一种新发现的检查点,其特征是在CD4+ T细胞、CD8+ T细胞、自然杀伤(NK)细胞、调节性T细胞(Tregs)和TIL(肿瘤浸润淋巴细胞)(TILs)上表达升高。迄今为止的研究表明,TIGIT在多种癌症中与NK细胞和T细胞的耗竭有关。CD155作为TIGIT在人类中的特异性配体,由于与TIGIT的关键相互作用,成为免疫治疗的重要靶点。此外,大量研究表明,TIGIT与其他免疫检查点抑制剂(ICIs)和/或传统治疗的联合在结直肠癌(CRC)中引发强效的抗肿瘤反应。本综述概述了TIGIT在多种免疫系统细胞类型中的结构、功能和信号通路。此外,本研究聚焦于TIGIT在CRC进展中的作用,回顾了探索基于TIGIT的免疫治疗在CRC中的各项研究。
The T cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domain (TIGIT), a newly discovered checkpoint, is characterized by its elevated expression on CD4 + T cells, CD8 + T cells, natural killer (NK) cells, regulatory T cells (Tregs), and tumor-infiltrating lymphocytes (TILs).
Research to date has been shown that TIGIT has been linked to exhaustion of NK cell both and T cells in numerous cancers. CD155, being the specific ligand of TIGIT in humans, emerges as a key target for immunotherapy owing to its crucial interaction with TIGIT.
Furthermore, numerous studies have demonstrated that the combination of TIGIT with other immune checkpoint inhibitors (ICIs) and/or traditional treatments elicits a potent antitumor response in colorectal cancer (CRC). This review provides an overview of the structure, function, and signaling pathways associated with TIGIT across multiple immune system cell types.
Additionally, focusing on the role of TIGIT in the progression of CRC, this study reviewed various studies exploring TIGIT-based immunotherapy in CRC.
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