IgE in the pathogenesis of asthmatic responses. Production of Th2-type cytokines (IL-4 and IL-13) by T cells in response to antigens like airborne allergens will drive IgE synthesis by B cells. IgE can then bind to high-affinity IgE receptors on mast cells. Cross-linking of the bound IgE molecules upon reexposure to the antigen provokes mast cell degranulation with the subsequent release of a variety of mediators, which trigger both early and late inflammatory asthmatic responses.