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Updated: Jun 17, 2026

Cultivation of Heligmosomoides Polygyrus: An Immunomodulatory Nematode Parasite and its Secreted Products
Published on: April 6, 2015
ILC3s promote intestinal tuft cell hyperplasia and anthelmintic immunity through RANK signaling
Hongkai Xu1,2,3, Yibo Wang1,2,3,4, Wenyan Wang2,4
1Institute for Immunology, Tsinghua University, Beijing 100084, China.
Helminth infections trigger a reprogramming of Group 3 innate lymphoid cells (ILC3s), enhancing immunity. These ILC3s, through RANKL, promote tuft cell expansion, boosting the immune response against helminths.
Area of Science:
- Immunology
- Infectious Diseases
- Gastroenterology
Background:
- Helminth infections pose a significant global health challenge, particularly in developing nations.
- Group 3 innate lymphoid cells (ILC3s) are key players in intestinal immunity against microbes but their role in helminth infections is unknown.
Purpose of the Study:
- To investigate the role of ILC3s in the host's immune response to intestinal helminth infection.
- To elucidate the mechanisms by which ILC3s contribute to anthelmintic immunity.
Main Methods:
- Analysis of ILC3 reprogramming during helminth infection.
- Investigating the function of ILC3-derived RANKL (receptor activator of NF-κB ligand) in synergy with IL-13.
- Assessing the impact of genetic deletion of RANKL, RANK, or RelB on tuft cell hyperplasia and anthelmintic immunity.
Main Results:
- Helminth infection reprograms ILC3s to promote anthelmintic immunity.
- ILC3-derived RANKL, in conjunction with IL-13, drives intestinal tuft cell expansion.
- Tuft cell expansion activates the tuft cell-ILC2 circuit, crucial for controlling helminth infection.
- Genetic ablation of RANKL in ILC3s or RANK/RelB in epithelial cells impairs tuft cell hyperplasia and weakens anti-helminth immunity.
Conclusions:
- ILC3s are essential for effective defense against helminth infections.
- ILC3s regulate intestinal tuft cell hyperplasia and type 2 immunity, crucial for helminth control.
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