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Neuropilin-1 mediates lung tissue-specific control of ILC2s function in type 2 immunity

ABSTRACT: ILC2s are highly heterogeneous tissue-resident lymphocytes that regulate inflammation and tissue homeostasis in health and disease. But how they integrate to the respective tissue microenvironment to perform tissue-supportive functions remain poorly defined. Here, we identify neuropilin-1, which is induced postnatally and sustained by lung-derived TGFβ1, as a tissue signature of lung ILC2s. Genetic ablation or pharmacological inhibition of Nrp1 suppresses ILC2s function and protects mice from the development of pulmonary fibrosis. Mechanistically, TGFβ1-Nrp1 signaling enhances ILC2s function and type 2 immunity through upregulation of IL-33 receptor ST2 expression. Our findings identify Nrp1 as a tissue-specific regulator of lung-resident ILC2s activation and highlight Nrp1 as a potential therapeutic target for pulmonary fibrosis

ORGANISM(S): Mus musculus

PROVIDER: GSE168809 | GEO | 2021/10/22

REPOSITORIES: GEO

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Nrp1 downregulation correlates with enhanced ILC2 responses during IL-33 challenge

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Neuropilin-1 mediates lung tissue-specific control of ILC2s function in type 2 immunity

Project description:Neuropilin-1 mediates lung tissue-specific control of ILC2s function in type 2 immunity

| PRJNA714077 | ENA

A proteomics approach to isolating neuropilin-dependent α5 integrin trafficking pathways: neuropilin 1 and 2 co-traffic α5 integrin through endosomal p120RasGAP to promote polarised fibronectin fibrillogenesis in endothelial cells

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