TLR4+group 2 innate lymphoid cells contribute to persistent type 2 immunity in airway diseases

Yan Li, Zaichuan Wang, Su Duan, Xue Wang, Yuling Zhang, Claus Bachert, Nan Zhang, Wei Wang, Sun Ying, Feng Lan (), Chengshuo Wang () and Luo Zhang ()
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Yan Li: Beijing Key Laboratory of New Medicine and Diagnostic Technology Research for Nasal Disease
Zaichuan Wang: Beijing Key Laboratory of New Medicine and Diagnostic Technology Research for Nasal Disease
Su Duan: Beijing Key Laboratory of New Medicine and Diagnostic Technology Research for Nasal Disease
Xue Wang: Beijing Key Laboratory of New Medicine and Diagnostic Technology Research for Nasal Disease
Yuling Zhang: Beijing Key Laboratory of New Medicine and Diagnostic Technology Research for Nasal Disease
Claus Bachert: University Hospital of Münster
Nan Zhang: Ghent University
Wei Wang: Capital Medical University
Sun Ying: Capital Medical University
Feng Lan: Beijing Key Laboratory of New Medicine and Diagnostic Technology Research for Nasal Disease
Chengshuo Wang: Beijing Key Laboratory of New Medicine and Diagnostic Technology Research for Nasal Disease
Luo Zhang: Beijing Key Laboratory of New Medicine and Diagnostic Technology Research for Nasal Disease

Nature Communications, 2025, vol. 16, issue 1, 1-17

Abstract: Abstract Group 2 innate lymphoid cells (ILC2s) directly contribute to local inflammation in type 2 inflammatory airway diseases. Here, we identify ILC2 subsets by single cell RNA sequencing in chronic rhinosinusitis with nasal polyps (CRSwNP) and in a memory inflammatory mouse model. We find that toll-like receptor 4 (TLR4)+ILC2s, with similar markers to their human counterparts, expresse memory cell markers, persist over time, and respond more vigorously to a secondary unrelated antigen challenge in the mouse model. Genetic ablation of TLR4 or blockade by anti-TLR4 antibodies leads to the reduction of IL-13 expression from ILC2s and mucus production in mice. The assay for transposase-accessible chromatin sequencing further confirms the importance of accessible TLR4 gene loci and its down-stream signaling pathway in maintaining trained immunity of TLR4+ILC2s after repeated stimulation by HDM. Taken together, TLR4 has a function in trained immunity maintenance within ILC2s, which may contribute to disease chronicity through a non-specific immunological memory.

Date: 2025
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DOI: 10.1038/s41467-025-62532-0

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