Neurogenic regulation of group 2 innate lymphoid cells in asthma

Abstract

Asthma is a chronic airways disorder characterized by reversible airflow limitation that is variable, airway hyperresponsiveness and bronchial inflammation and is associated with symptoms of wheeze, cough and productive mucus. Asthma can be phenotyped based on airway inflammation, where eosinophilic asthma is the most prevalent phenotype. Group 2 innate lymphoid cells (ILC2) play a central role in the pathogenesis of eosinophilic asthma by producing copious quantities of type 2 cytokines, such as IL-5 and IL-13, in an antigen-independent manner. ILC2 have been shown to promote airway inflammatory response in response to epithelial-derived cytokines (IL-25, IL-33, thymic stromal lymphopoietin and tumor necrosis factor-like peptide 1A (TL1A)), lipid mediators and hormones. Among soluble mediators, there is a growing body of data from murine and human studies showing that neurotransmitters and neuropeptides secreted by local nerve fibers contribute to the modulation of lung ILC2 activation in the pathogenesis of asthma. In this review, evidence supporting the relationship between ILC2 and neurogenic inflammation in asthma pathogenesis is discussed.