Food allergy

Abstract

Food allergies affect up to 6% of young children and 3%-4% of adults. They encompass a range of disorders that may be IgE and/or non-IgE mediated, including anaphylaxis, pollen food syndrome, food-protein-induced enterocolitis syndrome, food-induced proctocolitis, eosinophilic gastroenteropathies, and atopic dermatitis. Many complex host factors and properties of foods are involved in the development of food allergy. With recent advances in the understanding of how these factors interact, the development of several novel diagnostic and therapeutic strategies is underway and showing promise.

Figure 1. Mechanisms of oral tolerance.

(A) Generation of an immune response requires ligation of the T cell receptor with peptide-MHC complexes in the presence of appropriate costimulatory molecules (CD80 and CD86) and cytokines. (B) With high doses of oral antigen, T cell receptor cross-linking can occur in the absence of costimulation or in the presence of inhibitory ligands (CD95 and CD95 ligand), leading to anergy or deletion, respectively. (C) Low doses of oral antigen lead to the activation of regulatory T cells, which suppress immune responses through soluble or cell surface–associated suppressive cytokines (IL-10 and TGF-β). Adapted from ref. with permission from Elsevier.

Figure 2. Mean threshold dose of peanut flour eliciting symptoms in patients receiving Hu-901 or placebo.

The mean increase in the threshold of sensitivity, as compared with that in the placebo group, reached significance only in the 450-mg group (P < 0.001); however, results of the test for trend with increasing doses were significant (P < 0.001). Data show 95% confidence intervals. Adapted from ref. with permission from the Publishing Division of the Massachusetts Medical Society.