Interferon gamma constrains type 2 lymphocyte niche boundaries during mixed inflammation.

Autor:	Cautivo KM; Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA, USA., Matatia PR; Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA, USA., Lizama CO; Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, USA., Mroz NM; Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA, USA; Biomedical Sciences Graduate Program, University of California, San Francisco, San Francisco, CA, USA., Dahlgren MW; Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA, USA., Yu X; Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA, USA., Sbierski-Kind J; Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA, USA., Taruselli MT; Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA, USA., Brooks JF; Department of Medicine, University of California, San Francisco, San Francisco, CA, USA., Wade-Vallance A; Biomedical Sciences Graduate Program, University of California, San Francisco, San Francisco, CA, USA., Caryotakis SE; Biomedical Sciences Graduate Program, University of California, San Francisco, San Francisco, CA, USA., Chang AA; Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA, USA; Biomedical Sciences Graduate Program, University of California, San Francisco, San Francisco, CA, USA., Liang HE; Department of Medicine, University of California, San Francisco, San Francisco, CA, USA; Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA, USA., Zikherman J; Department of Medicine, University of California, San Francisco, San Francisco, CA, USA., Locksley RM; Department of Medicine, University of California, San Francisco, San Francisco, CA, USA; Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA, USA., Molofsky AB; Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA, USA; Diabetes Center, University of California, San Francisco, San Francisco, CA, USA. Electronic address: ari.molofsky@ucsf.edu.
Jazyk:	angličtina
Zdroj:	Immunity [Immunity] 2022 Feb 08; Vol. 55 (2), pp. 254-271.e7.
DOI:	10.1016/j.immuni.2021.12.014
Abstrakt:	Allergic immunity is orchestrated by group 2 innate lymphoid cells (ILC2s) and type 2 helper T (Th2) cells prominently arrayed at epithelial- and microbial-rich barriers. However, ILC2s and Th2 cells are also present in fibroblast-rich niches within the adventitial layer of larger vessels and similar boundary structures in sterile deep tissues, and it remains unclear whether they undergo dynamic repositioning during immune perturbations. Here, we used thick-section quantitative imaging to show that allergic inflammation drives invasion of lung and liver non-adventitial parenchyma by ILC2s and Th2 cells. However, during concurrent type 1 and type 2 mixed inflammation, IFNγ from broadly distributed type 1 lymphocytes directly blocked both ILC2 parenchymal trafficking and subsequent cell survival. ILC2 and Th2 cell confinement to adventitia limited mortality by the type 1 pathogen Listeria monocytogenes. Our results suggest that the topography of tissue lymphocyte subsets is tightly regulated to promote appropriately timed and balanced immunity. Competing Interests: Declaration of interests The authors declare no competing interests. (Copyright © 2021 Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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