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Oral Tolerance

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Part of the book series: Immunology and Medicine Series ((IMME,volume 29))

Abstract

A majority of the contacts with foreign antigenic materials occur at mucosal surfaces, which is larger than the area of the skin. The mucosal surface is constantly and physiologically exposed to a large variety of antigenic materials. Orally administered antigen encounters the gut associated lymphoid tissue (GALT) which has inherent property of not only to protect the host from ingested pathogens but also to prevent the host from reacting to ingested proteins. Thus, orally administered antigens induce systemic hyporesponsiveness to the fed proteins and this phenomenon termed oral tolerance. It was first described in 1911 when Wells fed hen egg proteins to guinea-pigs and found them resistant to anaphylaxis when challenged [1]. In 1946, Chase fed guinea pigs the contact-sensitizing agent dinitrochlorobenzene (DNCB) and observed that animals had decreased skin reactivity to DNCB [2]. It has also been observed in human fed and immunized with KLH [3]. There have been many studies trying to elucidate the mechanisms of oral tolerance [4, 5] and now it is clear that oral tolerance is mediated by T cells through different mechanisms depending on the dose of antigen fed. Low dose antigen favors the induction of regulatory T cells which suppress Th1 cell mediated response and high dose antigen induce T cell clonal anergy or deletion. In recent years, oral tolerance has been used successfully to treat autoimmune diseases in animal models and is now being applied to the treatment of human diseases.

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Weiner, H.L. (2001). Oral Tolerance. In: Thomson, A.W. (eds) Therapeutic Immunosuppression. Immunology and Medicine Series, vol 29. Springer, Dordrecht. https://doi.org/10.1007/978-94-010-0765-8_7

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