"Type 2 inflammation is characterized by overexpression and heightened activity of type 2 cytokines, mediators and cells that drive neuroimmune activation and sensitization to previously sub-threshold stimuli. The consequences of altered neuroimmune activity differ with tissue type and disease and include: skin inflammation, sensitization to pruritogens, and itch amplification in atopic dermatitis and prurigo nodularis; airway inflammation/hyperresponsiveness, loss of expiratory volume, airflow obstruction and increased mucus production in asthma; loss of sense of smell in chronic rhinosinusitis with nasal polyps; and dysphagia in eosinophilic esophagitis. We describe the neuroimmune interactions that underlie the various sensory and autonomic pathologies in type 2 inflammatory diseases and present recent advances in targeted treatment approaches to reduce type 2 inflammation and its associated symptoms in these diseases. Further research is needed to better understand the neuroimmune mechanisms that underlie chronic, sustained inflammation and its related sensory pathologies in diseases associated with type 2 inflammation."
ABPA, ACh, AD, ADCC, AFR, AHR, AR, ASM, Acetylcholine, Airway hyperresponsiveness, Airway smooth muscle, Allergic bronchopulmonary aspergillosis, Allergic fungal rhinosinusitis, Allergic rhinitis, Antibody-dependent cellular cytotoxicity, Atopic dermatitis, BAM8-22, BP, Beta chain, Bovine adrenal medulla peptide 8-22, Bullous pemphigoid, C-C motif chemokine ligand 17, CCL17, CGRP, CIU, COPD, CRSsNP, CRSwNP, CSF2, CSU, Calcitonin gene-related peptide, Chronic idiopathic urticaria, Chronic obstructive pulmonary disease, Chronic rhinosinusitis with nasal polyps, Chronic rhinosinusitis without nasal polyps, Chronic spontaneous urticaria, Colony stimulating factor 2, DRG, Dorsal root ganglion, EGPA, EMA, EoE, Eosinophilic esophagitis, Eosinophilic granulomatosis with polyangiitis, European Medicines Agency, FDA, FcεRIα, FeNO, Fractional exhaled nitric oxide, G-protein-coupled receptor, GPCR, Group 2 innate lymphoid cell, HES, High-affinity Fc receptor for IgE, Hypereosinophilic syndrome, IFNG-AS1, IFNγ, IL, IL-13R, IL-13Rα1/2, IL-1RαP, IL-31R, IL-31RA, IL-33R, IL-4Rα, IL-5Rα, ILC, ILC2, IRF1, IgE, Immunoglobulin E, Innate lymphoid cell, Interferon gamma-AS1, Interferon regulatory factor 1, Interferon-gamma, Interleukin, Interleukin-1 receptor alpha P, Interleukin-13 receptor, Interleukin-13 receptor alpha 1/2, Interleukin-31 receptor, Interleukin-31 receptor A, Interleukin-33 receptor, Interleukin-4 receptor alpha, Interleukin-5 receptor alpha, JAK, JAK inhibitors, JAKi, Janus kinase, MAPK, MCP-4, MRGPRX1, Mas-related family of G protein-coupled receptor 11, Mas-related family of G protein-coupled receptor X1, Mas-related family of G-protein-coupled receptor 3, Mas-related family of G-protein-coupled receptors, Mitogen-activated protein kinase, Monoclonal antibody, Monocyte chemoattractant protein-4, MrgprA, MrgprA3, MrgprCr11, NGF, NMU, NP, Na(v), Nasal polyps, Nerve growth factor, Neuromedin U, OSM, OSMRβ, Oncostatin M, Oncostatin-M specific receptor subunit beta, PAR2, PC(20), PN, Protease activated receptor 2, Provocative concentration causing a 20% drop in forced expiratory volume in 1 second from baseline, Prurigo nodularis, SP, STAT, Sialic-acid-binding immunoglobulin-like lectin 8, Signal transducer and activator of transcription, Substance P, T helper type 2 cell, TRP, TRPA1, TRPM4, TRPM8, TRPV1 TRPV4, TSLP, TSLPR, Th2, Thymic stromal lymphopoietin, Thymic stromal lymphopoietin receptor, Transient receptor potential, Transient receptor potential ankyrin 1, Transient receptor potential cation channel subfamily M member 4, Transient receptor potential cation channel subfamily M member 8, Transient receptor potential vanilloid 1, US Food and Drug Administration, VIP, Vasoactive intestinal peptide, Voltage-gated sodium channel, gamma chain, mAb, mIgE, membrane IgE, siglec-8, Βc, β2-adrenergic receptor, β2AR, γc.