CD23 dependent transcytosis of IgE and immune complex across the polarized human respiratory epithelial cells (141.20)

Abstract

Abstract IgE is frequently present in airway secretions and its level can be enhanced in human patients with allergic rhinitis and bronchial asthma. However, it remains completely unknown how IgE appears in the airway secretions. In this study, we showed that CD23 (FceRII) was expressed in the established or primary human airway epithelial cells; its expression was significantly up-regulated when airway epithelial cells were subjected to IL-4 stimulation. In a transcytosis assay, CD23 was capable of transporting IgE across the polarized human Calu-3 monolayer in a bidirectional manner. Furthermore, CD23 was able to transport IgE derived immune complexes. CD23 specific antibody or soluble CD23 significantly reduced the efficiency of IgE or immune complex transcytosis, suggesting a specific receptor-mediated transport by CD23. Exposure of Calu-3 monolayer to IL-4 also enhanced the transcytosis of either human IgE or the immune complex. Transcytosis of both IgE and the immune complex was further verified in primary human airway epithelial cell monolayers. Furthermore, the transcytosed immune complexes were competent in inducing degranulation of the cultured human mast cells. Since airway epithelial cells are the first cell layer to come into contact with inhaled allergens, our study implies CD23-mediated IgE transcytosis in human airway epithelial cells may play a critical role in initiating and contributing to the perpetuation of airway allergic inflammation.