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:Unveiling the multifaceted antitumor effects of interleukin 33.
Unveiling the multifaceted antitumor effects of interleukin 33.
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。
白细胞介素33(IL-33)曾主要因其促肿瘤活性而被认识,如今已成为一种具有抗肿瘤特性的多功能细胞因子。IL-33的多效性活性包括激活Th1 CD4+ T细胞、CD8+ T细胞、NK细胞、树突状细胞、嗜酸性粒细胞以及2型固有淋巴细胞。就这种免疫调节活性而言,IL-33与多种癌症治疗手段表现出协同相互作用,包括免疫检查点阻断和化疗。利用IL-33的联合治疗在不同肿瘤模型中展现出增强的抗肿瘤疗效,为癌症治疗提供了新的有前景的途径。尽管IL-33具有抗肿瘤效应,但其在肿瘤微环境中的复杂相互作用凸显了进一步研究的必要性。理解IL-33作为肿瘤进展促进者和抑制者双重角色背后的机制,对于完善治疗策略和充分实现其在癌症免疫治疗中的潜力至关重要。本综述深入探讨了IL-33在肿瘤微环境中作用的复杂图景,强调其在协调抗肿瘤免疫应答中的关键作用。
Interleukin 33 (IL-33), once predominantly recognized for its pro-tumoral activities, has emerged as a multifunctional cytokine with antitumor properties. IL-33 pleiotropic activities include activation of Th1 CD4 + T cells, CD8 + T cells, NK cells, dendritic cells, eosinophils, as well as type 2 innate lymphoid cells. Regarding this immunomodulatory activity, IL-33 demonstrates synergistic interactions with various cancer therapies, including immune checkpoint blockade and chemotherapy. Combinatorial treatments leveraging IL-33 exhibit enhanced antitumor efficacy across different tumor models, promising novel avenues for cancer therapy.
Despite its antitumor effects, the complex interplay of IL-33 within the tumor microenvironment underscores the need for further investigation. Understanding the mechanisms underlying IL-33's dual role as both a promoter and inhibitor of tumor progression is essential for refining therapeutic strategies and fully realizing its potential in cancer immunotherapy. This review delves into the intricate landscape of IL-33 effects within the tumor microenvironment, highlighting its pivotal role in orchestrating immune responses against cancer.
在 PubMed 查看 → 出版商原文(DOI) 全文 PDF(PMC)· 可下载 治疗专题与资料阅读指南 资料来源与翻译说明 报告译文或资料问题 →
MEMBER ACCOUNT
登录成功会直接打开下一页。