Feeding antigens to experimental animals can result in oral tolerance, a peripheral immunological non-responsiveness induced by the processing of exogenous antigen through gut associated lymphoid tissue.1 Oral administration of autoantigen has been shown to ameliorate disease in a number of rodent models of organ specific autoimmune conditions including experimental autoimmune uveoretinitis (EAU),1-5 experimental autoimmune encephalomyelitis (EAE),6 experimental granulomatous colitis,7and experimental autoimmune thyroiditis.8 Because antigen feeding protocols have been shown to be effective even in sensitised recipients with established disease, induction of oral tolerance represents a novel potential strategy for the treatment of human autoimmune disease, allergy and possibly graft rejection.

The mechanisms involved in induction and maintenance of oral tolerance depend critically upon antigen dosage.13 Immunisation with high doses of antigen leads to energy of antigen reactive cells, whereas lower antigen doses induce a form of immune deviation or active suppression. Anergy reflects the situation in which antigen reactive cells are generated but are functionally inactive: the molecular mechanisms involved are uncertain. Immune deviation operates through induction of a population of transforming growth factor beta …