Host-derived lipids orchestrate pulmonary γδ T cell response to provide early protection against influenza virus infection

Xiaohui Wang (), Xiang Lin, Zihan Zheng, Bingtai Lu, Jun Wang, Andy Hee-Meng Tan, Meng Zhao, Jia Tong Loh, Sze Wai Ng, Qian Chen, Fan Xiao, Enyu Huang, King-Hung Ko, Zhong Huang, Jingyi Li, Kin-Hang Kok, Gen Lu, Xiaohui Liu, Kong-Peng Lam, Wanli Liu, Yuxia Zhang, Kwok-Yung Yuen, Tak Wah Mak and Liwei Lu ()
Additional contact information
Xiaohui Wang: The University of Hong Kong
Xiang Lin: The University of Hong Kong
Zihan Zheng: Chongqing International Institute for Immunology
Bingtai Lu: Guangzhou Medical University
Jun Wang: Guangzhou Medical University
Andy Hee-Meng Tan: Agency for Science, Technology and Research
Meng Zhao: Tsinghua University
Jia Tong Loh: Agency for Science, Technology and Research
Sze Wai Ng: Agency for Science, Technology and Research
Qian Chen: The University of Hong Kong
Fan Xiao: The University of Hong Kong
Enyu Huang: The University of Hong Kong
King-Hung Ko: The University of Hong Kong
Zhong Huang: Shenzhen University School of Medicine
Jingyi Li: Chongqing International Institute for Immunology
Kin-Hang Kok: The University of Hong Kong
Gen Lu: Guangzhou Medical University
Xiaohui Liu: Tsinghua University
Kong-Peng Lam: Agency for Science, Technology and Research
Wanli Liu: Tsinghua University
Yuxia Zhang: Guangzhou Medical University
Kwok-Yung Yuen: The University of Hong Kong
Tak Wah Mak: The University of Hong Kong
Liwei Lu: The University of Hong Kong

Nature Communications, 2021, vol. 12, issue 1, 1-19

Abstract: Abstract Innate immunity is important for host defense by eliciting rapid anti-viral responses and bridging adaptive immunity. Here, we show that endogenous lipids released from virus-infected host cells activate lung γδ T cells to produce interleukin 17 A (IL-17A) for early protection against H1N1 influenza infection. During infection, the lung γδ T cell pool is constantly supplemented by thymic output, with recent emigrants infiltrating into the lung parenchyma and airway to acquire tissue-resident feature. Single-cell studies identify IL-17A-producing γδ T (Tγδ17) cells with a phenotype of TCRγδhiCD3hiAQP3hiCXCR6hi in both infected mice and patients with pneumonia. Mechanistically, host cell-released lipids during viral infection are presented by lung infiltrating CD1d+ B-1a cells to activate IL-17A production in γδ T cells via γδTCR-mediated IRF4-dependent transcription. Reduced IL-17A production in γδ T cells is detected in mice either lacking B-1a cells or with ablated CD1d in B cells. Our findings identify a local host-immune crosstalk and define important cellular and molecular mediators for early innate defense against lung viral infection.

Date: 2021
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DOI: 10.1038/s41467-021-22242-9

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