Pulmonary environmental cues drive group 2 innate lymphoid cell dynamics in mice and humans.

Autor:	Puttur F; Inflammation, Repair and Development, National Heart and Lung Institute, Imperial College London, London, UK., Denney L; Inflammation, Repair and Development, National Heart and Lung Institute, Imperial College London, London, UK., Gregory LG; Inflammation, Repair and Development, National Heart and Lung Institute, Imperial College London, London, UK., Vuononvirta J; Inflammation, Repair and Development, National Heart and Lung Institute, Imperial College London, London, UK., Oliver R; Inflammation, Repair and Development, National Heart and Lung Institute, Imperial College London, London, UK., Entwistle LJ; Inflammation, Repair and Development, National Heart and Lung Institute, Imperial College London, London, UK., Walker SA; Inflammation, Repair and Development, National Heart and Lung Institute, Imperial College London, London, UK., Headley MB; Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA., McGhee EJ; Cancer Research UK Beatson Institute, Garscube Estate, Bearsden, Glasgow, UK., Pease JE; Inflammation, Repair and Development, National Heart and Lung Institute, Imperial College London, London, UK., Krummel MF; Department of Pathology, University of California, San Francisco, 513 Parnassus Ave., San Francisco, CA, USA., Carlin LM; Inflammation, Repair and Development, National Heart and Lung Institute, Imperial College London, London, UK. c.lloyd@imperial.ac.uk l.carlin@beatson.gla.ac.uk.; Cancer Research UK Beatson Institute, Garscube Estate, Bearsden, Glasgow, UK.; Institute of Cancer Sciences, University of Glasgow, Glasgow, UK., Lloyd CM; Inflammation, Repair and Development, National Heart and Lung Institute, Imperial College London, London, UK. c.lloyd@imperial.ac.uk l.carlin@beatson.gla.ac.uk.
Jazyk:	angličtina
Zdroj:	Science immunology [Sci Immunol] 2019 Jun 07; Vol. 4 (36).
DOI:	10.1126/sciimmunol.aav7638
Abstrakt:	Group 2 innate lymphoid cells (ILC2s) are enriched in mucosal tissues (e.g., lung) and respond to epithelial cell-derived cytokines initiating type 2 inflammation. During inflammation, ILC2 numbers are increased in the lung. However, the mechanisms controlling ILC2 trafficking and motility within inflamed lungs remain unclear and are crucial for understanding ILC2 function in pulmonary immunity. Using several approaches, including lung intravital microscopy, we demonstrate that pulmonary ILC2s are highly dynamic, exhibit amoeboid-like movement, and aggregate in the lung peribronchial and perivascular spaces. They express distinct chemokine receptors, including CCR8, and actively home to CCL8 deposits located around the airway epithelium. Within lung tissue, ILC2s were particularly motile in extracellular matrix-enriched regions. We show that collagen-I drives ILC2 to markedly change their morphology by remodeling their actin cytoskeleton to promote environmental exploration critical for regulating eosinophilic inflammation. Our study provides previously unappreciated insights into ILC2 migratory patterns during inflammation and highlights the importance of environmental guidance cues in the lung in controlling ILC2 dynamics. (Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.)
Databáze:	MEDLINE
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