Group 2 innate lymphoid cells and eosinophilic chronic rhinosinusitis

Purpose of review Chronic rhinosinusitis (CRS) is a heterogeneous disease and is recently classified into two phenotypes, eosinophilic CRS (ECRS) and non-ECRS. ECRS is characterized by Th2-biased eosinophilic inflammation, and non-ECRS is characterized by Th1-biased neutrophilic inflammation. Group 2 innate lymphoid cells (ILC2s) rapidly produce large amounts of Th2 cytokines and exert critical roles in Th2-type immune responses. We summarize our current knowledge about the pathogenic roles of ILC2s in ECRS. Recent findings The prevalence of ILC2s is increased in nasal polyps, and it is positively correlated with the number of infiltrating eosinophils. Epithelium-derived cytokines (IL-33, IL-25, and thymic stromal lymphopoietin), cysteinyl leukotrienes, and prostaglandin D-2 stimulate the production of Th2 cytokines from ILC2s, which drives eosinophilic inflammation in nasal mucosa. Regulation of ILC2s would be a novel therapeutic approach for the refractory and/or recurrent cases of ECRS. Increased ILC2s play a pivotal role in the pathophysiology of ECRS by producing large amounts of Th2 cytokines, which lead to Th2-type eosinophilic inflammation in nasal polyps.