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:Interplay between inflammasomes and PD-1/PD-L1 and their implications in cancer immunotherapy.
Interplay between inflammasomes and PD-1/PD-L1 and their implications in cancer immunotherapy.
分数与星级只用于站内排序 —— 不代表疗效、安全性或个人适用性。
炎症小体在炎症和癌症发展中起着至关重要的作用,而 PD-1/PD-L1 通路对于肿瘤微环境(TME)中的免疫抑制至关重要。近年来的研究表明,在癌症发展和 PD-1 阻断治疗中,炎症小体与 PD-1/PD-L1 信号传导之间存在相互调控关系。炎症小体通过在肿瘤组织中的多种细胞中激活,上调 TME 中 PD-L1 的水平。此外,炎症小体激活对 PD-1/PD-L1 活性的调控涉及NK 细胞、肿瘤相关巨噬细胞和髓源性抑制细胞。反之,PD-1 阻断可以激活炎症小体,可能影响治疗结果。炎症小体与 PD-1/PD-L1 之间的相互作用对癌症发展和治疗具有深远而复杂的影响。在这篇综述中,我们讨论了癌症中炎症小体与 PD-1/PD-L1 之间的串扰,探讨了它们对肿瘤发生、转移和免疫检查点抑制剂(ICI)耐药的意义。同时靶向炎症小体和检查点分子的联合治疗策略具有作为癌症治疗的广阔潜力。
The inflammasomes play crucial roles in inflammation and cancer development, while the PD-1/PD-L1 pathway is critical for immune suppression in the tumor microenvironment (TME). Recent research indicates a reciprocal regulatory relationship between inflammasomes and PD-1/PD-L1 signaling in cancer development and PD-1 blockade treatment. By activating in diverse cells in tumor tissues, inflammasome upregulates PD-L1 level in the TME.
Moreover, the regulation of PD-1/PD-L1 activity by inflammasome activation involves natural killer cells, tumor-associated macrophages and myeloid-derived suppressor cells. Conversely, PD-1 blockade can activate the inflammasome, potentially influencing treatment outcomes. The interplay between inflammasomes and PD-1/PD-L1 has profound and intricate effects on cancer development and treatment.
In this review, we discuss the crosstalk between inflammasomes and PD-1/PD-L1 in cancers, exploring their implications for tumorigenesis, metastasis and immune checkpoint inhibitor (ICI) resistance. The combined therapeutic strategies targeting both inflammasomes and checkpoint molecules hold promising potential as treatments for cancer.
MEMBER ACCOUNT
登录成功会直接打开下一页。