免疫系统
多不饱和脂肪酸
mTORC1型
细胞生物学
生物
自然杀伤细胞
免疫检查点
化学
细胞毒性T细胞
Wnt信号通路
细胞毒性
癌细胞
癌症研究
白细胞介素12
细胞
白细胞介素21
Janus激酶3
淋巴因子激活杀伤细胞
免疫监视
癌症免疫疗法
肿瘤微环境
糖酵解
免疫
T细胞
作者
Yi Luan,Chuan Yang,Hongyue Zhou,Zhuo Chen,Ao Li,Peng Liu,Dianqing Wu,Wenwen Tang
出处
期刊:Science Signaling
[American Association for the Advancement of Science]
日期:2026-08-11
卷期号:19 (950): eady2865-eady2865
标识
DOI:10.1126/scisignal.ady2865
摘要
Polyunsaturated fatty acids (PUFAs) play a crucial role in tumor development by influencing not only tumor cells but also immune cells within the tumor microenvironment. Here, we explored the mechanisms by which PUFAs are transported and function within immune cells to regulate tumor growth. We found that PUFA transport through LDL receptor-related protein 5 (LRP5) into natural killer (NK) cells played an essential role in modulating the cells' antitumor function. LRP5 deficiency or expression of LRP5 lacking the LDLa domain enhanced the cytotoxicity and antitumor activity of NK cells both in vivo and in culture. However, wild-type NK cells cultured in the absence of PUFAs and NK cells from mice fed a PUFA-free diet also exhibited enhanced cytotoxicity, eliminating the functional difference between wild-type and NK cells expressing LDLa domain-deficient LRP5. Mechanistically, LRP5-mediated PUFA transport suppressed mTORC1 signaling and glycolysis in NK cells, a metabolic pathway essential for NK cell cytotoxicity. Thus, our study identified LRP5 as an immune checkpoint that restrains NK cell activity through PUFA transport-dependent suppression of mTORC1 signaling.
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