Unknown

Dataset Information

0

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


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.

SUBMITTER: Wang X 

PROVIDER: S-EPMC7997921 | biostudies-literature |

REPOSITORIES: biostudies-literature

Similar Datasets

| S-EPMC6431623 | biostudies-literature
| S-EPMC4352080 | biostudies-literature
| S-EPMC4309539 | biostudies-literature
| S-EPMC5944318 | biostudies-literature
| S-EPMC7519780 | biostudies-literature
| S-EPMC8086055 | biostudies-literature
| S-EPMC7168235 | biostudies-literature
| S-EPMC6465541 | biostudies-literature
| S-EPMC8764156 | biostudies-literature
| S-EPMC3831310 | biostudies-literature