Interferon gamma constrains type 2 lymphocyte niche boundaries during mixed inflammation
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 simila...
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creator | Cautivo, Kelly M Matatia, Peri R Lizama, Carlos O Mroz, Nicholas M Dahlgren, Madelene W Yu, Xiaofei Sbierski-Kind, Julia Taruselli, Marcela T Brooks, Jeremy F Wade-Vallance, Adam Caryotakis, Sofia E Chang, Anthony A Liang, Hong-Erh Zikherman, Julie Locksley, Richard M Molofsky, Ari B |
description | 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. |
doi_str_mv | 10.1016/j.immuni.2021.12.014 |
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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.</description><identifier>ISSN: 1074-7613</identifier><identifier>EISSN: 1097-4180</identifier><identifier>DOI: 10.1016/j.immuni.2021.12.014</identifier><identifier>PMID: 35139352</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Cell Death - immunology ; Cell Movement - immunology ; Hypersensitivity - immunology ; Immunity, Innate ; Inflammation - immunology ; Interferon-gamma - immunology ; Interleukin-33 - immunology ; Interleukin-5 - metabolism ; Listeria monocytogenes ; Listeriosis - immunology ; Listeriosis - mortality ; Liver - immunology ; Lung - immunology ; Lymphocyte Subsets - immunology ; Lymphocyte Subsets - metabolism ; Lysophospholipids - immunology ; Mice ; Parenchymal Tissue - immunology ; Sphingosine - analogs & derivatives ; Sphingosine - immunology ; Th1 Cells - immunology ; Th2 Cells - immunology ; Th2 Cells - metabolism</subject><ispartof>Immunity (Cambridge, Mass.), 2022-02, Vol.55 (2), p.254-271.e7</ispartof><rights>Copyright © 2021 Elsevier Inc. 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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. 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subjects | Animals Cell Death - immunology Cell Movement - immunology Hypersensitivity - immunology Immunity, Innate Inflammation - immunology Interferon-gamma - immunology Interleukin-33 - immunology Interleukin-5 - metabolism Listeria monocytogenes Listeriosis - immunology Listeriosis - mortality Liver - immunology Lung - immunology Lymphocyte Subsets - immunology Lymphocyte Subsets - metabolism Lysophospholipids - immunology Mice Parenchymal Tissue - immunology Sphingosine - analogs & derivatives Sphingosine - immunology Th1 Cells - immunology Th2 Cells - immunology Th2 Cells - metabolism |
title | Interferon gamma constrains type 2 lymphocyte niche boundaries during mixed inflammation |
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