Environmental Ligands of the Aryl Hydrocarbon Receptor in Allergic Rhinitis: Immune and Neuroimmune Mechanisms
- 1School of Clinical Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu 610075, China
Abstract
Allergic rhinitis (AR) is an immunoglobulin E (IgE)-mediated chronic inflammatory disease. Although type 2 immune responses are central to AR, environmental exposures, epithelial barrier dysfunction, and neuroimmune interactions also contribute to disease development. The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that links environmental signals to immune responses. Elevated AhR expression in peripheral blood mononuclear cells from patients with AR has been associated with clinical severity. In non-AR experimental systems, AhR suppresses histamine-associated interleukin-6 (IL-6) production in macrophages, whereas 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) reduces acetylcholinesterase (AChE) expression and activity in neuronal cells. These findings suggest possible links to nasal inflammation and cholinergic regulation, but their contribution to nasal symptoms in AR remains to be established. In addition, AhR modulates mast-cell, B-cell, and T-cell responses in a ligand- and cell-dependent manner. Overall, AhR may exert protective or pathogenic effects depending on the activating ligand and target cell type, suggesting that its therapeutic potential in AR lies in ligand- and cell-specific modulation.
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BibTeX
@article{xiong2026environmental,
title = {{Environmental Ligands of the Aryl Hydrocarbon Receptor in Allergic Rhinitis: Immune and Neuroimmune Mechanisms}},
author = {Yalan Xiong and Jia Han and Zhaoxin Yang and Yongqin Liu and Peiwen Ding and Xinyi Bian and Bohua Yan and Yu Fang},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = oct,
doi = {10.3390/ijms27219545},
url = {https://www.mdpi.com/1422-0067/27/21/9545},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Environmental Ligands of the Aryl Hydrocarbon Receptor in Allergic Rhinitis: Immune and Neuroimmune Mechanisms
AU - Yalan Xiong
AU - Jia Han
AU - Zhaoxin Yang
AU - Yongqin Liu
AU - Peiwen Ding
AU - Xinyi Bian
AU - Bohua Yan
AU - Yu Fang
PY - 2026
DA - 2026/10/26
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27219545
UR - https://www.mdpi.com/1422-0067/27/21/9545
AB - Allergic rhinitis (AR) is an immunoglobulin E (IgE)-mediated chronic inflammatory disease. Although type 2 immune responses are central to AR, environmental exposures, epithelial barrier dysfunction, and neuroimmune interactions also contribute to disease development. The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that links environmental signals to immune responses. Elevated AhR expression in peripheral blood mononuclear cells from patients with AR has been associated with clinical severity. In non-AR experimental systems, AhR suppresses histamine-associated interleukin-6 (IL-6) production in macrophages, whereas 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) reduces acetylcholinesterase (AChE) expression and activity in neuronal cells. These findings suggest possible links to nasal inflammation and cholinergic regulation, but their contribution to nasal symptoms in AR remains to be established. In addition, AhR modulates mast-cell, B-cell, and T-cell responses in a ligand- and cell-dependent manner. Overall, AhR may exert protective or pathogenic effects depending on the activating ligand and target cell type, suggesting that its therapeutic potential in AR lies in ligand- and cell-specific modulation.
SN - 1422-0067
ER -