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RIPK1 作为增强 DC 在肿瘤免疫治疗中疗效的潜在靶点

英文原题:RIPK1 as a potential target to augment DC efficacy in tumor immunotherapy.

查看英文原题

RIPK1 as a potential target to augment DC efficacy in tumor immunotherapy.

PubMed 2026/03/17(内容时间) Cancer Immunol Immunother Q1 · IF 5.8(JCR 2025)

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中文摘要

基于树突状细胞(DC)的疫苗是一种具有巨大潜力的肿瘤免疫治疗方法,提高其疗效是亟待解决的问题。RIPK1是炎症和细胞死亡的重要调节因子,可能在DC的肿瘤免疫功能中发挥重要作用。我们的研究发现,DC特异性敲除Ripk1可通过增加DC免疫浸润和加强肿瘤微环境中与细胞毒性T细胞的相互作用来抑制小鼠肿瘤生长。DC特异性Ripk1敲除的疗效也在体外实验中得到验证,揭示了Ripk1敲除的功能涉及增强DC的抗原呈递能力和活化状态及其激活Cd8+ T细胞的能力。此外,这种Ripk1敲除的DC疫苗被用于治疗荷瘤小鼠,与野生型DC疫苗相比,它能有效抑制肿瘤生长。RIPK1有望成为提高DC疫苗疗效的新靶点。

展开英文摘要原文

Dendritic Cell (DC)-based vaccine is a tumor immunotherapy approach with great potential, and improving the efficacy is an urgent problem to be solved. RIPK1 is an important regulator of inflammation and cell death, and may play a significant role in the tumor immune function of DCs.

Our study found that DC-specific knockout of Ripk1 can inhibit tumor growth in mice by increasing DC immune infiltration and strengthening the interactions with cytotoxic T cells in the tumor microenvironment. The efficacy of DC-specific Ripk1 knockout was also validated in in vitro experiments, revealing the function of the Ripk1 knockout involved augment of antigen presentation capacity and activation status of DCs and their ability to activate Cd8 + T cells.

Furthermore, this Ripk1 knocked DCs vaccine was employed to treat the tumor carry mice and it can effectively inhibit tumor growth compared with the wild type DCs vaccine. RIPK1 is expected to become a new target for improving the efficacy of DC vaccines.

论文信息

作者
Mao L、Ou Y、Zhang Y、Wang M、Dong G、Khanniche A、Wang H、Wu Z
第一作者单位
Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.China
通讯作者单位
Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, 200031, China. xykong@sinh.ac.cn.China
期刊
Cancer immunology, immunotherapy : CII2026 Mar 17
原文标识
PubMed 41843169 · DOI 10.1007/s00262-026-04356-5