Allergic rhinitis(AR)is the most common airway allergic diseases.Basophils are the classical effector cells in allergy,including AR:Both IgE and non-IgE mediated methods can activate basophils during allergic reactions and induce basophils to release various inflammatory mediators,which is accompanied by changes in the expression of multiple membrane proteins,and ulti-mately leading to the clinical manifestations of allergic diseases.IL-18 may be involved in the pathogenesis of AR by directly inducing basophil activation and inflammation response via binding to its receptor IL-18Rα.Nevertheless,the binding of IL-37b to IL-18Rα initiates the downstream anti-inflammatory signals,thus inhibiting inflammation reaction in AR.Therefore,understanding the role and mechanism of IL-18 and IL-37b in the activation of blood basophils of AR patients is of great significance for the pathogenesis,treat-ment of AR and the development of related biological agents.

Allergic rhinitis(AR)is the most common airway allergic diseases.Basophils are the classical effector cells in allergy,including AR:Both IgE and non-IgE mediated methods can activate basophils during allergic reactions and induce basophils to release various inflammatory mediators,which is accompanied by changes in the expression of multiple membrane proteins,and ulti-mately leading to the clinical manifestations of allergic diseases.IL-18 may be involved in the pathogenesis of AR by directly inducing basophil activation and inflammation response via binding to its receptor IL-18Rα.Nevertheless,the binding of IL-37b to IL-18Rα initiates the downstream anti-inflammatory signals,thus inhibiting inflammation reaction in AR.Therefore,understanding the role and mechanism of IL-18 and IL-37b in the activation of blood basophils of AR patients is of great significance for the pathogenesis,treat-ment of AR and the development of related biological agents.

Objective:To investigate the expression of IL-18, IL-18-binding protein a(IL-18BPa) and IL-18 receptor α(IL-18Rα) by peripheral blood CD4 + Th17 cells of patients with allergic rhinitis (AR) and the effects of allergens on their expression. Methods:This study enrolled 45 outpatients with AR and 23 healthy control subjects receiving physical examination in the First Affiliated Hospital of Jinzhou Medical University from October 2019 to September 2020. According to the results of skin prick test, the 45 patients were divided into two groups: AR group with positive results (24 cases) and nAR group with negative results (21 cases). Blood samples of them were collected. Flow cytometry was used to analyze the effects of allergens on the expression of IL-18, IL-18BPa and IL-18Rα at protein level by peripheral blood CD4 + Th17 cells. The level of IL-17A in plasma was measured by Bioplex system, and its correlation with the percentage of IL-18 + Th17 cells was analyzed. Results:Compared with the healthy control group, the AR group showed increased ratios of CD4 + Th17 and IL-18 + Th17 cells ( P<0.01), decreased ratio of IL-18BPa + Th17 cells ( P<0.01), enhanced mean fluorescence intensity (MFI) of IL-18BPa ( P<0.01) and reduced MFI of IL-18Rα ( P<0.01); the nAR group showed enhanced MFI of IL-18BPa ( P<0.000 1) and reduced MFI of IL-18Rα ( P<0.000 1). The ratio of IL-18 + Th17 cells and the MFI of IL-18Rα in the AR group were higher than those in the nAR group ( P<0.05, P<0.01). House dust mite extract and Platanus pollen extract induced the expression of IL-18 and IL-18BPa by CD4 + Th17 cells of AR patients ( P<0.05). Moreover, house dust mite extract directly induced the CD4 + Th17 cells isolated from the healthy control subjects to express IL-18 and IL-18R ( P<0.05). Compared with healthy control subjects, AR patients had higher level of IL-17A in plasma and it was moderately correlated with the ratio of IL-18 + Th17 cells ( P<0.05). Conclusions:Allergens may be involved in the pathogenesis of AR by inducing blood CD4 + Th17 cells to express IL-18 and IL-18Rα.