Oral tolerance is very much the norm. The reason why we are not all allergic and intolerant when we eat food is due to basic mechanisms that function in the development of our tolerance. Food intolerance and food allergy is in fact a failure of oral tolerance. The existence of oral tolerance has been known for a long time, but its mechanisms are still not fully understood. A number of experimental models have been used to demonstrate this phenomenon. One such example is the oral tolerance to ovalbumin in mice. This was induced by a single administration of ovalbumin and a demonstration of suppression of cellmediated immunity.23
T-helper cells are differentiated into two subsets, known as Th1 cells and Th2 cells. Th1 cells produce cytokines such as gamma-interferon and induce macrophage activation. In the absence of gamma-interferon, the antigen-presenting cells express another cytokine, IL-10, and induce Th2 cells to produce IL-4 cytokines. The latter cytokines will instruct naive B-cells to produce IgE. The balance between gamma-interferon and IL-4 at the time of the immune reaction will govern the immune outcome. High interferon/IL-4 production facilitates the induction of a Thl-type immune response, whereas high IL-4 production induces a Th2 pathway. In oral tolerance, it is suggested that T-helper cells known as Th3 type are involved. These cells, which produce TGF-/31, may be responsible for oral tolerance, since TGF-^1 downregulate inflammatory cytokines and promote IgA production.24
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