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:Promising New Anti-TIGIT Agents: Stealthy Allies in Cancer Immunotherapy.
Promising New Anti-TIGIT Agents: Stealthy Allies in Cancer Immunotherapy.
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TIGIT(含免疫球蛋白和酪氨酸抑制基序[ITIM]结构域的T细胞免疫受体)、Vstm3和VSIG9是新近受到关注的免疫检查点,在CD4+和CD8+ T细胞、TIL(肿瘤浸润淋巴细胞)、自然杀伤(NK)细胞及调节性T细胞(Treg)上均有明显表达。TIGIT蛋白对免疫调节至关重要,因为它会减少癌症患者及实验模型中的NK细胞群体,并抑制T细胞活性。CD155是TIGIT在人类中的主要配体,因与TIGIT相互作用而成为关键免疫治疗靶点。即使没有TIGIT表达,CD155仍与抗程序性死亡蛋白1(PD-1)治疗疗效相关,凸显其在免疫检查点抑制中的重要性。抗TIGIT药物单独使用或与抗PD-1联合,均显示增强恶性肿瘤免疫应答的潜力。本综述探讨TIGIT蛋白的结构和功能特征、抗TIGIT药物新进展及其在癌症免疫治疗中的潜在应用。
TIGIT (T cell immunoreceptor with immunoglobulin and tyrosine-based inhibitory motif (ITIM) domain), Vstm3, and VSIG9, are newly recognized immunological checkpoints. They are prominently expressed on CD4+ and CD8+ T cells, tumor-infiltrating lymphocytes (TILs), natural killer (NK) cells, and regulatory T cells (Tregs). The TIGIT (TIGIT) protein is crucial for immune modulation since it diminishes NK cell populations and hinders T cell activity in cancer patients and experimental models. CD155, the principal ligand of TIGIT in humans, has been recognized as a pivotal target for immunotherapy owing to its interaction with TIGIT.
CD155 is linked to the efficacy of anti-programmed cell death protein 1 (PD-1) therapy, even without TIGIT expression, underscoring its importance in immune checkpoint suppression. Anti-TIGIT medicines, either independently or in conjunction with anti-PD-1 treatments, have demonstrated potential in augmenting immune responses to malignancies. This review examines the structural and functional characteristics of the TIGIT protein, new developments in anti-TIGIT drugs, and their prospective use in cancer immunotherapy.
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