Activation of group 2 innate lymphoid cells after allergen challenge in asthmatic patients.


Journal

The Journal of allergy and clinical immunology
ISSN: 1097-6825
Titre abrégé: J Allergy Clin Immunol
Pays: United States
ID NLM: 1275002

Informations de publication

Date de publication:
07 2019
Historique:
received: 13 07 2018
revised: 13 01 2019
accepted: 22 01 2019
pubmed: 8 2 2019
medline: 19 5 2020
entrez: 8 2 2019
Statut: ppublish

Résumé

Group 2 innate lymphoid cells (ILC2s) are effective producers of IL-5 and IL-13 during allergic inflammation and bridge the innate and adaptive immune responses. ILC2 numbers are increased in asthmatic patients compared with healthy control subjects. Thus far, human data describing their phenotype during acute allergic inflammation in the lung are incomplete. This study aims to characterize and compare blood- and lung-derived ILC2s before and after segmental allergen challenge in patients with mild-to-moderate asthma with high blood eosinophil counts (≥300 cells/μL). ILC2s were isolated from blood and bronchoalveolar lavage (BAL) fluid before and after segmental allergen challenge. Cells were sorted by means of flow cytometry, cultured and analyzed for cytokine release or migration, and sequenced for RNA expression. ILC2s were nearly absent in the alveolar space under baseline conditions, but numbers increased significantly after allergen challenge (P < .05), whereas at the same time, ILC2 numbers in blood were reduced (P < .05). Prostaglandin D ILC2s accumulate at the site of allergic inflammation and are recruited from the blood. Their transcriptional and functional activation pattern promotes type 2 inflammation.

Sections du résumé

BACKGROUND
Group 2 innate lymphoid cells (ILC2s) are effective producers of IL-5 and IL-13 during allergic inflammation and bridge the innate and adaptive immune responses. ILC2 numbers are increased in asthmatic patients compared with healthy control subjects. Thus far, human data describing their phenotype during acute allergic inflammation in the lung are incomplete.
OBJECTIVES
This study aims to characterize and compare blood- and lung-derived ILC2s before and after segmental allergen challenge in patients with mild-to-moderate asthma with high blood eosinophil counts (≥300 cells/μL).
METHODS
ILC2s were isolated from blood and bronchoalveolar lavage (BAL) fluid before and after segmental allergen challenge. Cells were sorted by means of flow cytometry, cultured and analyzed for cytokine release or migration, and sequenced for RNA expression.
RESULTS
ILC2s were nearly absent in the alveolar space under baseline conditions, but numbers increased significantly after allergen challenge (P < .05), whereas at the same time, ILC2 numbers in blood were reduced (P < .05). Prostaglandin D
CONCLUSION
ILC2s accumulate at the site of allergic inflammation and are recruited from the blood. Their transcriptional and functional activation pattern promotes type 2 inflammation.

Identifiants

pubmed: 30731124
pii: S0091-6749(19)30184-8
doi: 10.1016/j.jaci.2019.01.027
pii:
doi:

Substances chimiques

Allergens 0
Antigens, Dermatophagoides 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

61-69.e7

Informations de copyright

Copyright © 2019. Published by Elsevier Inc.

Auteurs

Carla Winkler (C)

Respiratory, Inflammation and Autoimmunity, Biotech IMED Unit, AstraZeneca, Gothenburg, Sweden. Electronic address: carla.winkler@astrazeneca.com.

Thomas Hochdörfer (T)

Respiratory, Inflammation and Autoimmunity, Biotech IMED Unit, AstraZeneca, Gothenburg, Sweden.

Elisabeth Israelsson (E)

Respiratory, Inflammation and Autoimmunity, Biotech IMED Unit, AstraZeneca, Gothenburg, Sweden.

Annemarie Hasselberg (A)

Respiratory, Inflammation and Autoimmunity, Biotech IMED Unit, AstraZeneca, Gothenburg, Sweden.

Anders Cavallin (A)

Respiratory, Inflammation and Autoimmunity, Biotech IMED Unit, AstraZeneca, Gothenburg, Sweden.

Kristofer Thörn (K)

Respiratory, Inflammation and Autoimmunity, Biotech IMED Unit, AstraZeneca, Gothenburg, Sweden.

Daniel Muthas (D)

Respiratory, Inflammation and Autoimmunity, Biotech IMED Unit, AstraZeneca, Gothenburg, Sweden.

Shervin Shojaee (S)

Discovery Science, Biotech IMED Unit, AstraZeneca, Gothenburg, Sweden.

Katrin Lüer (K)

Fraunhofer Institute of Toxicology and Experimental Medicine, Hannover, Germany.

Meike Müller (M)

Fraunhofer Institute of Toxicology and Experimental Medicine, Hannover, Germany.

Jenny Mjösberg (J)

Center for Infectious Diseases, Karolinska Institute, Stockholm, Sweden; Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.

Outi Vaarala (O)

Respiratory, Inflammation and Autoimmunity, Biotech IMED Unit, AstraZeneca, Gothenburg, Sweden.

Jens Hohlfeld (J)

Fraunhofer Institute of Toxicology and Experimental Medicine, Hannover, Germany; Member of the German Center for Lung Research (BREATH), Hannover, Germany; Department of Respiratory Medicine, Hannover Medical School, Hannover, Germany.

Katerina Pardali (K)

Respiratory, Inflammation and Autoimmunity, Biotech IMED Unit, AstraZeneca, Gothenburg, Sweden.

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Classifications MeSH