| LKB1 prevents ILC2 exhaustion to enhance antitumor immunity | |
| 論文作者 | Niu, HS; Zhang, HS; Wang, DD; Zhao, LF; Zhang, YQ; Zhou, WY; Zhang, JJ; Su, XH; Sun, JP; Su, B; Qiu, J; Shen, L |
| 期刊/會(huì)議名稱(chēng) | CELL REPORTS |
| 論文年度 | 2024 |
| 論文類(lèi)別 | |
| 摘要 | Group 2 innate lymphoid cells (ILC2s) play crucial roles in mediating allergic inflammation. Recent studies also indicate their involvement in regulating tumor immunity. The tumor suppressor liver kinase B1 (LKB1) inactivating mutations are associated with a variety of human cancers; however, the role of LKB1 in ILC2 function and ILC2-mediated tumor immunity remains unknown. Here, we show that ablation of LKB1 in ILC2s results in an exhausted -like phenotype, which promotes the development of lung melanoma metastasis. Mechanistically, LKB1 deficiency leads to a marked increase in the expression of programmed cell death protein -1 (PD -1) in ILC2s through the activation of the nuclear factor of activated T cell pathway. Blockade of PD -1 can restore the effector functions of LKB1-deficient ILC2s, leading to enhanced antitumor immune responses in vivo . Together, our results reveal that LKB1 acts to restrain the exhausted state of ILC2 to maintain immune homeostasis and antitumor immunity. |
| 期 | 5 |
| 卷 | 43 |
| 影響因子 | 7.5 |
官方微信
