Abstract
The lung is constantly exposed to environmental particulates such as aeroallergens, pollutants, or microorganisms and is protected by a poised immune response. Innate lymphoid cells (ILCs) are a population of immune cells found in a variety of tissue sites, particularly barrier surfaces such as the lung and the intestine. ILCs play a crucial role in the innate immune system, and they are involved in the maintenance of mucosal homeostasis, inflammation regulation, tissue remodeling, and pathogen clearance. In recent years, group 3 innate lymphoid cells (ILC3s) have emerged as key mediators of mucosal protection and repair during infection, mainly through IL-17 and IL-22 production. Although research on ILC3s has become focused on the intestinal immunity, the biology and function of pulmonary ILC3s in the pathogenesis of respiratory infections and in the development of chronic pulmonary inflammatory diseases remain elusive. In this review, we will mainly discuss how pulmonary ILC3s act on protection against pathogen challenge and pulmonary inflammation, as well as the underlying mechanisms.
Highlights
The lung is constantly exposed to particulates such as aeroallergens, pollutants, or microorganisms from the external environment
Similar to the findings in helminthic lung infections, ST2+ natural ILC2s (nILC2s) are defined in the lung inflammation induced by papain or IL-33, which possesses some characteristics of group 3 innate lymphoid cells (ILC3s), for example, aryl hydrocarbon receptor (AhR) expression and IL-17 production (Cai et al, 2019)
While research studies on ILC3s have become a focus in the intestinal immunity (Withers and Hepworth, 2017; Pantazi and Powell, 2019), the biology and function of pulmonary ILC3s in the pathogenesis of respiratory diseases remain elusive
Summary
The lung is constantly exposed to particulates such as aeroallergens, pollutants, or microorganisms from the external environment. The key role of IL-23 and IL-1b in ILC3 activation has been confirmed in lung infection (Van Maele et al, 2014; Muir et al, 2016; Trevejo-Nunez et al, 2016; Ardain et al, 2019) and airway inflammatory diseases (Kim et al, 2014; Everaere et al, 2016; Shikhagaie et al, 2017; Yanagisawa et al, 2017; Komlosi et al, 2018; Kim et al, 2019; Lee et al, 2020).
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