IgE-Fc epsilonRI-mast cell axis in the allergic cycle.

The IgE and allergen dependent activation of mast cells via the high affinity IgE receptor (Fc epsilonRI) resulting in the release of inflammatory mediators is critical to the pathogenesis of atopic diseases like bronchial asthma and allergic rhinitis. However, mast cells are also involved in certain IgE-independent biological responses, and recent studies have highlighted the role of mast cells in host defense. In the light of this background, we have discussed our recent data on the immunophenotypic characteristics of nasal mast cells in patients with perennial allergic rhinitis (PAR) and chronic infective rhinitis (CIR) based on the expression of cytokines, the Fc epsilonRI, the cell-bound IgE, as well as the IgE-mediated mediator release (before and after saturation of the IgE receptors). Although nasal mast cells (NMC) from both groups of patients expressed a variety of cytokines, significant differences were observed in the proportion of cytokine expressing cells between PAR and CIR. NMC from PAR patients exhibited increased Fc epsilonRI expression, cell-bound IgE and IgE-mediated mediator release as compared with NMC from CIR patients, even after saturation of the IgE receptors. The density of IgE receptors and IgE molecules in NMC of PAR patients correlated well with the levels of serum IgE, and IL-4 upregulated the expression of the Fc epsilonRI in NMC. Moreover, NMC from PAR patients induced IgE synthesis in B cells. Taken together, these results and the recently demonstrated IgE-induced upregulation of the Fc epsilonRI expression in mast cells suggest critical roles for mast cells in promoting the allergic reaction through an IgE-Fc epsilonRI-mast cell axis.