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Interferon gamma constrains type 2 lymphocyte niche boundaries during mixed inflammation

Cautivo, Kelly M ; Matatia, Peri R ; Lizama, Carlos O ; Mroz, Nicholas M ; Dahlgren, Madelene W LU orcid ; Yu, Xiaofei ; Sbierski-Kind, Julia ; Taruselli, Marcela T ; Brooks, Jeremy F and Wade-Vallance, Adam , et al. (2022) In Immunity 55(2). p.7-271
Abstract

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... (More)

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.

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publishing date
type
Contribution to journal
publication status
published
keywords
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, Liver/immunology, Lung/immunology, Lymphocyte Subsets/immunology, Lysophospholipids/immunology, Mice, Parenchymal Tissue/immunology, Sphingosine/analogs & derivatives, Th1 Cells/immunology, Th2 Cells/immunology
in
Immunity
volume
55
issue
2
pages
7 - 271
publisher
Cell Press
external identifiers
  • scopus:85124014549
  • pmid:35139352
ISSN
1074-7613
DOI
10.1016/j.immuni.2021.12.014
language
English
LU publication?
no
additional info
Copyright © 2021 Elsevier Inc. All rights reserved.
id
361193a8-c3c2-443d-b173-f1ed43b609ba
date added to LUP
2024-05-06 00:00:02
date last changed
2024-05-20 06:34:40
@article{361193a8-c3c2-443d-b173-f1ed43b609ba,
  abstract     = {{<p>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.</p>}},
  author       = {{Cautivo, Kelly M and Matatia, Peri R and Lizama, Carlos O and Mroz, Nicholas M and Dahlgren, Madelene W and Yu, Xiaofei and Sbierski-Kind, Julia and Taruselli, Marcela T and Brooks, Jeremy F and Wade-Vallance, Adam and Caryotakis, Sofia E and Chang, Anthony A and Liang, Hong-Erh and Zikherman, Julie and Locksley, Richard M and Molofsky, Ari B}},
  issn         = {{1074-7613}},
  keywords     = {{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; Liver/immunology; Lung/immunology; Lymphocyte Subsets/immunology; Lysophospholipids/immunology; Mice; Parenchymal Tissue/immunology; Sphingosine/analogs & derivatives; Th1 Cells/immunology; Th2 Cells/immunology}},
  language     = {{eng}},
  month        = {{02}},
  number       = {{2}},
  pages        = {{7--271}},
  publisher    = {{Cell Press}},
  series       = {{Immunity}},
  title        = {{Interferon gamma constrains type 2 lymphocyte niche boundaries during mixed inflammation}},
  url          = {{http://dx.doi.org/10.1016/j.immuni.2021.12.014}},
  doi          = {{10.1016/j.immuni.2021.12.014}},
  volume       = {{55}},
  year         = {{2022}},
}