Antibody Fc-receptor FcεR1γ stabilizes cell surface receptors in group 3 innate lymphoid cells and promotes anti-infection immunity

Chao Huang (), Wenting Zhu, Qing Li, Yuchen Lei, Xi Chen, Shaorui Liu, Dianyu Chen, Lijian Zhong, Feng Gao, Shujie Fu, Danyang He, Jinsong Li and Heping Xu ()
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Chao Huang: University of Chinese Academy of Sciences
Wenting Zhu: Westlake University
Qing Li: University of Chinese Academy of Sciences
Yuchen Lei: University of Chinese Academy of Sciences
Xi Chen: Westlake University
Shaorui Liu: Westlake University
Dianyu Chen: Westlake University
Lijian Zhong: University of Chinese Academy of Sciences
Feng Gao: Westlake University
Shujie Fu: Westlake University
Danyang He: Westlake University
Jinsong Li: University of Chinese Academy of Sciences
Heping Xu: Westlake University

Nature Communications, 2024, vol. 15, issue 1, 1-15

Abstract: Abstract Group 3 innate lymphoid cells (ILC3) are crucial for maintaining mucosal homeostasis and regulating inflammatory diseases, but the molecular mechanisms governing their phenotype and function are not fully understood. Here, we show that ILC3s highly express Fcer1g gene, which encodes the antibody Fc-receptor common gamma chain, FcεR1γ. Genetic perturbation of FcεR1γ leads to the absence of critical cell membrane receptors NKp46 and CD16 in ILC3s. Alanine scanning mutagenesis identifies two residues in FcεR1γ that stabilize its binding partners. FcεR1γ expression in ILC3s is essential for effective protective immunity against bacterial and fungal infections. Mechanistically, FcεR1γ influences the transcriptional state and proinflammatory cytokine production of ILC3s, relying on the CD16-FcεR1γ signaling pathway. In summary, our findings highlight the significance of FcεR1γ as an adapter protein that stabilizes cell membrane partners in ILC3s and promotes anti-infection immunity.

Date: 2024
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DOI: 10.1038/s41467-024-50266-4

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