Neurogenic regulation of group 2 innate lymphoid cells in asthma
- 1Respiratory Research Group, Department of Medicine, McMaster University
- 2Department of Pulmonary Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University
- 3Firestone Institute for Respiratory Health, St. Joseph’s Healthcare
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.
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BibTeX
@article{matsuyama2026neurogenic,
title = {{Neurogenic regulation of group 2 innate lymphoid cells in asthma}},
author = {Takahiro Matsuyama and Nahal Emami Fard and Akimichi Nagashima and Roma Sehmi},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1927691},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1927691/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Neurogenic regulation of group 2 innate lymphoid cells in asthma
AU - Takahiro Matsuyama
AU - Nahal Emami Fard
AU - Akimichi Nagashima
AU - Roma Sehmi
PY - 2026
DA - 2026/10/05
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1927691
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1927691/full
AB - 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.
SN - 1664-3224
ER -