ABSTRACT
Pathogenesis In the case of IgE-mediated reactions, prior sensitization to the allergen is necessary. Upon subsequent exposure to even a minute quantity of the offending substance, the antigen or the allergen cross-links with the high-affinity FcR1 receptor on the surface of the mast cell or basophil and induces degranulation and release of preformed and newly formed mediators (histamine, prostaglandin D2 and tryptase) that are responsible for the reaction. These mediators induce smooth muscle contraction, vasodilatation and increased capillary permeability, and also cause chemotaxis of other inflammatory cells. In some cases, the allergen/antigen binds covalently to a low molecular protein (hapten) and the specific IgE is
directed against this complex. In cases of non-IgE-mediated reaction, the activation of mast cells occurs via the formation of immune complexes, the activation of complement or coagulation pathways or it is kinin-mediated. Figure 5.1 summarizes the various agents known to induce anaphylactic reactions together with their underlying mechanisms.
