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^–, CD11b^bright) 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.