Journal Article

Physiological microbial exposure transiently inhibits mouse lung ILC2 responses to allergens

Iijima, Koji, Kucaba, Tamara A, Griffith, Thomas S, Tei, Rinna, Pierson, Mark J, Xu, Julie, Staley, Christopher, Khan, Mohammad Haneef, Block, Katharine E, Walsh, Daniel A, Jameson, Stephen C, Kita, Hirohito, McSorley, Henry J

2022

Overview

Lung group 2 innate lymphoid cells (ILC2s) control the nature of immune responses to airway allergens. Some microbial products, including those that stimulate interferons, block ILC2 activation, but whether this occurs after natural infections or causes durable ILC2 inhibition is unclear. In the present study, we cohoused laboratory and pet store mice as a model of physiological microbial exposure. Laboratory mice cohoused for 2 weeks had impaired ILC2 responses and reduced lung eosinophilia to intranasal allergens, whereas these responses were restored in mice cohoused for ≥2 months. ILC2 inhibition at 2 weeks correlated with increased interferon receptor signaling, which waned by 2 months of cohousing. Reinduction of interferons in 2-month cohoused mice blocked ILC2 activation. These findings suggest that ILC2s respond dynamically to environmental cues and that microbial exposures do not control long-term desensitization of innate type 2 responses to allergens.Here the authors show that mice exposed to a variety of pathogens initially have impaired innate type 2 responses to lung allergens, but reactivity resets over time, indicating that microbial experience does not stably inhibit innate immunity to allergens.

• Publisher: Nature Publishing Group
• Subject: Allergens / Eosinophilia / Immune response / Innate immunity / Interferon / Laboratories / Laboratory animals / Lungs / Lymphoid cells / Physiology