Abstract
Animal models of food allergy have been used to identify mechanisms involved in the development of sensitization to food proteins as well as immunologic mechanisms of adverse reactions to allergen reexposure. To counteract the normal tolerant responses to antigen generated in the gastrointestinal tract, investigators have used mucosal adjuvants or manipulated the mucosal barrier, taken advantage of endogenous adjuvanticity of some food allergens, or bypassed the oral route and sensitized through the skin. Site of antigen uptake in the gastrointestinal tract is a critical factor in both sensitization and anaphylaxis, and antigen uptake can be facilitated by immunoglobulin-E (IgE)–antigen complexes binding to CD23 on the epithelial cell surface. Studies on systemic anaphylaxis or local gastrointestinal manifestations of food allergy in mice have highlighted the contribution of IgE, mast cells, and pathogenic Th2 lymphocytes in experimental food allergy.
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