The gastrointestinal tract plays an important role in the mucosal immune response. While acting as a conduit allowing the transfer of nutrients from the intestinal lumen to the systemic circulation, it also protects against invasion by microbes and other antigens by the induction of an immune response. A downregulation of these immune responses to nonharmful antigenic substances is termed oral tolerance. A breakdown or underdevelopment of oral tolerance may therefore lead to the development of food allergy. Adverse immunologic reactions to food may be a consequence of both IgE- and non-IgE-mediated mechanisms. Although genetic factors play a major role in the development of allergic disease, other factors involved in an immature mucosal immune response have been implicated. Non-IgE-mediated allergic responses tend to involve a T cell-mediated delayed hypersensitivity reaction, and released cytokines act as determinants of the immune response. The "hygiene hypothesis" proposes that a reduction in infections in early infancy predisposes to allergic responses. Early childhood infections promote the induction of a T-helper type 1 response that protects against the development of allergy, which is predominantly a T-helper type 2 response. The role of B cells and T cells in the development of food allergy is incompletely under- stood, but advances in the evaluation and characterization of food allergens has opened exciting new avenues in this study.