IGE-FC-EPSILON-RI MAST-CELL AXIS IN THE ALLERGIC CYCLE

The IgE and allergen dependent activation of mast cells via the high a ffinity IgE receptor (Fc epsilon RI) resulting in the release of infla mmatory mediators is critical to the pathogenesis of atopic diseases l ike bronchial asthma and allergic rhinitis. However, mast cells;are al so involved in certain IgE-independent biological responses, and recen t studies have highlighted the role of mast cells in host defense. In the light of this background, we have dis cussed our recent data on th e immunophenotypic characteristics of nasal mast cells in patients wit h perennial allergic rhinitis (PAR) and chronic infective rhinitis (CI R) based on the expression of cytokines, the FceRI, the cell-bound IgE , as well as the IgE-mediated mediator release (before and after satur ation of the IgE receptors). Although nasal mast cells (NMC) from both groups of patients expressed a variety of cytokines, significant diff erences were observed in the proportion of cytokine expressing cells b etween PAR and CIR. NMC from PAR patients exhibited increased Fc epsil on RI 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 PA R patients correlated well with the levels of serum IgE, and IL-4 upre gulated the expression of the Fc epsilon RI 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 FceRI expression in mast cells suggest critical roles for mast cells i n promoting the allergic reaction through an IgE-Fc epsilon RI-mast ce ll axis.