Oral tolerance in disease

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Abstract
The large surface area of the gastrointestinal tract is covered by a single layer of columnar epithelium which allows efficient absorption of nutrients, but also offers a potential portal of entry for microbial pathogens. Thus, a highly structured immune network, the GALT has evolved as an integral part of the intestine to provide protection against pathogenetic microorganisms.1 However, the intestinal immune system is faced with the dilemma of discriminating between antigens with no pathogenetic potential (dietary proteins and commensal organisms) and antigens associated with potentially harmful microbes. It has long been recognised that the encounter of dietary antigens by the immune system normally leads to antigen specific tolerance.2 This phenomenon has been termed oral tolerance and can be induced by most soluble antigens.3 , 4 The consequences of the apparent breakdown of oral tolerance to dietary antigens are exemplified by diseases such as gluten sensitive enteropathy (coeliac disease) and other food sensitive enteropathies.4 The intestinal immune system must also maintain stringent control over responses to its resident bacterial flora. These organisms are essential for normal intestinal function, yet they constitute a potential challenge to the integrity of the host. Recent evidence suggests that the breakdown of intestinal immunoregulation of responses to endogenous flora may be the underlying cause of inflammatory bowel diseases such as ulcerative colitis and Crohn’s disease.5-8 Understanding the mechanisms responsible for oral tolerance may lead to new treatment strategies for such conditions. In addition, antigen feeding may provide a potential immunotherapy for a number of systemic inflammatory disorders.
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