Distinct Roles of LFA-1 and ICAM-1 on ILC2s Control Lung Infiltration, Effector Functions, and Development of Airway Hyperreactivity.

Frontiers in Immunology
Benjamin P HurrellOmid Akbari

Abstract

Asthma is a heterogeneous airway inflammatory disease characterized by increased airway hyperreactivity (AHR) to specific and unspecific stimuli. Group 2 innate lymphoid cells (ILC2)s are type-2 cytokine secreting cells capable of inducing eosinophilic lung inflammation and AHR independent of adaptive immunity. Remarkably, reports show that ILC2s are increased in the blood of human asthmatics as compared to healthy donors. Nevertheless, whether ILC2 expression of adhesion molecules regulates ILC2 trafficking remains unknown. Our results show that IL-33-activated ILC2s not only express LFA-1 but also strikingly LFA-1 ligand ICAM-1. Both LFA-1-/- and ICAM-1-/- mice developed attenuated AHR in response to IL-33 intranasal challenge, associated with a lower airway inflammation and less lung ILC2 accumulation compared to controls. Our mixed bone marrow chimera studies however revealed that ILC2 expression of LFA-1 - but not ICAM-1 - was required for their accumulation in the inflamed lungs. Importantly, we found that LFA-1 remarkably controlled ILC2 homing to the lungs, suggesting that LFA-1 is involved in ILC2 trafficking to the lungs. Our exploratory transcriptomic analysis further revealed that ICAM-1 deficiency on ILC2s signific...Continue Reading

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Citations

Apr 17, 2021·Frontiers in Immunology·Hui SunBing Ni
Jun 29, 2021·Frontiers in Immunology·Haocheng ZhengTieshan Wang

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Datasets Mentioned

BETA
GSE158652

Methods Mentioned

BETA
flow cytometry
ELISA
RNAseq
Fluorescence
bronchoalveolar

Software Mentioned

GraphPad
FlowJo
GSA
Prism
STAR
Partek Genomics Suite

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