| ILC3s promote intestinal tuft cell hyperplasia and anthelmintic immunity through RANK signaling |
| 論文作者 |
Xu, HK; Wang, YB; Wang, WY; Fu, YX; Qiu, J; Shi, Y; Yuan, L; Dong, C; Hu, XY; Chen, YG; Guo, XH |
| 期刊/會(huì)議名稱 |
SCIENCE IMMUNOLOGY |
| 論文年度 |
2025 |
| 論文類別 |
|
| 摘要 |
Helminth infections, particularly in developing countries, remain a notable health burden worldwide. Group 3 innate lymphoid cells (ILC3s) are enriched in the intestine and play a critical role in immunity against extracellular bacteria and fungi. However, whether ILC3s are involved in intestinal helminth infection is still unclear. Here, we report that helminth infection reprograms ILC3s, which, in turn, promote anthelmintic immunity. ILC3-derived RANKL [receptor activator of NF-kappa B (nuclear factor kappa B) ligand] synergizes with interleukin-13 (IL-13) to facilitate intestinal tuft cell expansion after helminth infection, which further activates the tuft cell-group 2 innate lymphoid cell (ILC2) circuit to control helminth infection. Deletion of RANKL in ILC3s or deletion of RANK or its downstream adaptor RelB in intestinal epithelial cells substantially diminishes tuft cell hyperplasia and dampens anthelmintic immunity. Thus, ILC3s play an indispensable role in protecting against helminth infection through the regulation of intestinal tuft cell hyperplasia and type 2 immunity. |
| 卷 |
10 |
| 影響因子 |
16.3 |
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