CD23 on B cells determines Breg-facilitated IL-10 secretion as well as activation of T cells

Abstract

Objective:To explore whether or not the IL-10 mediated by Bregs modulate the secreting T cells activation by the anti-CD23 antibody, to find a new target for the treatment of allergic rhinitis. Method:The rat model of allergic rhinitis was established. Anti-CD23 antibody was used to observe the behavioral changes, passive skin allergen test, enzyme-linked immunosorbent assay, hematoxylin and eosin staining, immunofluorescence and flow cytometry serological indicators, systemic and nasal mucosa. Result:Compared with the blank control group, allergic rhinitis group rats sneezing, flexible nose, runny nose, subcutaneous mass increases;The levels of IL-10, IFN-γ and Bregs in blood decreased, the levels of IL-4, CD23+ B cells and CD4+ T cells increased;Nasal mucosa CD23 fluorescence intensity increased, CD19 and IL-10 fluorescence intensity decreased. Compared with the allergic rhinitis group, the number of sneezing, the frequency of nasal flexion, the symptoms of runny nose and the subcutaneous mass in the antibody intervention group were significantly improved;The levels of IL-10 in the blood, IFN-γ, the percentage of Bregs cells in whole blood increased, the levels of IL-4, CD23+ B cells and CD4+ T cells decreased;Nasal mucosa CD23 fluorescence intensity decreased, CD19 and IL-10 fluorescence intensity increased. There is little difference between the two routes of administration. Conclusion:The enhanced expression of CD23 on B cells is involved in the development of allergic rhinitis. The anti-CD23 antibody may control the symptoms and signs of allergic rhinitis. There is no significant difference between subcutaneous administration and improved nasal-drip way. As the preferred method of anti-CD23 antibody application, anti-CD23 is expected to become a new method to control and treat allergic rhinitis. Anti-CD23 antibodies can exert a therapeutic effect by T cell activation,which rely on the Bregs-mediated secretion of IL-10.