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

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 inflamm

SUBMITTER: Hurrell BP 

PROVIDER: S-EPMC7662114 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature