Cellular and cytokine feedback loops promoting IgE production in the allergic respiratory mucosa. APCs, preformed IgE, and a permissive cytokine milieu may all help predispose to Th2 responses in the bronchial mucosa of atopic individuals. Dendritic cells (DC) of the myeloid phenotype (CD8–, CD11bbright) favor the generation of Th2 cytokines. Allergen-specific IgE, usually present in atopic individuals, can passively sensitize B cells via the low-affinity IgE receptor CD23 and enhance the antigen-presenting capacity of these cells by several logs. Antigen presentation by B cells favors Th2 responses. The local production of IL-4 in the bronchial mucosa by multiple cell types enhances Th2 expansion. In addition to the preestablished allergen-specific Th2 T cells resident in the bronchial mucosa of allergic patients, possible sources of IL-4 include NK1.1 cells (both T and non-T) and mast cells. IL-4 production by mast cells is favored if they are sensitized, via FcεRI, by preformed IgE specific for the allergen. IL-4 supports the differentiation and expansion of allergen-specific Th2 cells, which then provide 2 signals, IL-4 and CD40L, that drive IgE production by B cells.