The asthmatic response is intiated when dendritic cells recognize the presence of an allergen. Through a process which is dependent on several leukocyte markers (CD3, CD4, and CD28) dendritic cells stimulate differentiation of naïve T cells into T helper type 2 cells (Th2), which release IL-4. The hallmark Th2 cytokine, IL-4 promotes clonal expansion and, along with IL-13 and specific co-stimulatory molecules, induces B cells to produce allergen-specific IgE antibodies. B cell-Th2 cell interactions require CD3, CD28, CD40, CD80 and CD86.
IgE antibodies subsequently bind to the Fc epsilon RI high affinity receptors found on mast cells, basophils, neutrophils, and eosinophils. Upon allergen re-exposure, allergen binding to the IgE-Fc epsilon RI complexes on mast cells and basophils leads to receptor cross-linking which triggers the release of mediators that cause immediate hypersensitivity during the early phase asthmatic reaction.