Figure 1.

Activation of MCs occurs when allergen specific IgE is bound by the allergen and interacts with the high affinity receptor for immunoglobulin (IgE), referred to as FcεRI, carried on their surfaces in the presence of mutations and other molecular-genetic defects. This culminates in the release of preformed and newly synthesized mediators from mast cells and basophils that sets off a sequence of inflammatory events manifesting clinically as anaphylaxis and leading to shock. MC-derived cytokines, histamine, leukotrienes, prostanoids, and PAF regulate vascular instability and barrier dysfunction of endothelial cells and contribute to edema formation. Hypovolemia, angioedema, hypotension, and cardiorespiratory failure ensue. Inset shows examples of urticaria and angioedema.