Study On Th17/Treg Cells In The Pathogenesis Of Allergic Rhinitis

Objective: AR is caused by the introduction of allergens into the nasal mucosa of specific individuals,stimulating the local production of specific antibodies,which then bind to specific cells,when the nasal mucosa again contact with the corresponding allergen,it immediately and antibody reaction,produce a variety of inflammatory substances,and then specific individuals produce the corresponding symptoms.In recent years,the incidence of allergic rhinitis in China has been increasing and getting younger,which has puzzled people’s study,work and life.However,the current treatment methods for allergic rhinitis can only control the basic symptoms of the patients,failed to cure the disease.In recent years,the single Th1/Th2 cell immune model has been extended to Th1/Th2/Thl7/Treg cell immune model.However,the specific relationship between the distribution of these T cells and their production of immune-related factors and the development of allergy has not been clearly elucidated.In this study,we analyzed the distribution of Th17/Treg cells in AR patients,and detected the levels of cytokines related to Th17/Treg cells,in order to further explore the relationship between the distribution of Th17/Treg cells and related cytokines,we focus on the regulation of Il-33 and Il-35 on Thl7/Treg cells in the pathogenesis of AR,which provides the basis for elucidating the signal pathway of AR and obtaining effective drug-controlled targets.Methods:From February 2019 to November 2020,40 patients with allergic rhinitis in North Jiangsu People’s Hospital were selected as experimental group and 30 healthy volunteers as control group.Treg cells and TH17 cells in peripheral blood were detected by Flow cytometry,cytokines were detected by ELISA,and the data were further analyzed by SPSS 20.0.Results : 1.The levels of Treg cells and Th17 cells in control group and experimental groupThe percentage of Treg cells in AR patients(14.4 ± 2.99%)was significantly lower than that in control group(21.03 ± 2.63%),and the percentage of Th17 cells(5.45 ±0.99%)was significantly higher than that in control group(3.19 ± 0.67%).2.Th17/Treg ratio in peripheral blood of control group and experimental groupTh17/Treg cell ratio(0.39 ± 0.12)in AR patients was significantly higher than that in control group(0.15 ± 0.39),and the difference was statistically significant(p <0.05).3.Changes and correlation of T cell-related cytokines in peripheral blood of experimental groupCompared with the control group,the serum levels of IL-9 and Il-13 in Th2 related Proinflammatory cytokine were significantly increased,and the serum levels of Il-17 and IL-25 in Th17 related Proinflammatory cytokine were significantly increased,the levels of Il-33 and Il-35 in Treg cells were significantly higher than those in Proinflammatory cytokine cells(p < 0.05),and the levels of Il-35 were significantly lower than those in Treg cells(p < 0.05)There was a negative correlation between Il-17 and Il-33(r =-0.432,p = 0.005).There was a negative correlation between Il-17 and Il-35(r =-0.362,P = 0.02).4.Correlation between T cell-associated cytokines and TREG/TH17 cellsThere was a negative correlation between IL-35 and TH17 cells,and the correlation was statistically significant(r =-0.358,P = 0.023).There was no clear correlation between other T cell-related cytokines and TREG/TH17 cells.Conclusion:1.The difference of Th17 cells and Treg cells existed in AR patients: the increase of Th17 cells,the decrease of Treg cells resulted in the abnormal distribution of Th17/Treg cells,and then the ratio of Th17/Treg cells increased significantly;2.There were abnormal expression of Th17 cells and Treg cells in AR patients: TH17 cells had a hyperinflammatory effect,Treg cells had a suppression of immune tolerance,and Th2 cytokines and TH17 related cytokines were increased,treg cell related factor secretion decreased;3.The changes of cytokines such as IL-33 and IL-35 may be closely related to the difference of Th17 cells and Treg cells distribution and abnormal function in AR patients,it is suggested that inhibition of IL-33 expression and promotion of IL-35 expression may be a new approach for AR therapy.