ABSTRACT
The physiopathology of the allergic immune responses is complex and influenced by several factors, including genetic susceptibility, route of exposure, allergen dose, and in some cases the structural characteristics of the allergen (1). The allergic immune response requires sensitization and development of specific immune response toward the allergen. During sensitization to allergen, priming of allergen-specific CD4+ T helper 2 (Th2) cells results in the production of Th2 cytokines [such as interleukin-4 (IL-4) and IL-13] that are responsible for class switching to the e heavy chain for IgE production by B cells, mucus production and activation of endothelial cells for Th2 cell, and eosinophil migration to tissues (2,3). IgE sensitizes mast cells and basophils by binding to the high-affinity receptor for IgE (FceRI) expressed on their surface. Upon cross-linking of the IgE-FceRI complexes by allergen, mast cells and basophils degranulate, releasing vasoactive amines (principally histamine), lipid mediators (prostaglandins and cysteinyl leukotrienes), cytokines and chemokines, all of which characterize the immediate phase of the allergic reaction (2,3).
