Abstract
The pathogenesis of Crohn's disease (CD) and ulcerative colitis (UC), the two main forms of inflammatory bowel disease (IBD), is still unclear, but both autoimmune and immune-mediated phenomena are involved. Autoimmune phenomena include the presence of serum and mucosal autoantibodies against intestinal epithelial cells in either form of IBD, and against human tropomyosin fraction five selectively in UC. In addition, perinuclear antineutrophil cytoplasmic antibodies (pANCA) are common in UC, whereas antibodies against Saccharomyces cerevisiae (ASCA) are frequently found in CD. Immune-mediate phenomena include a variety of abnormalities of humoral and cell-mediated immunity, and a generalized enhanced reactivity against intestinal bacterial antigens in both CD and UC. It is currently believed that loss of tolerance against the indigenous enteric flora is the central event in IBD pathogenesis. Various complementary factors probably contribute to the loss of tolerance to commensal bacteria in IBD. They include defects in regulatory T-cell function, excessive stimulation of mucosal dendritic cells, infections or variants of proteins critically involved in bacterial antigen recognition, such as the products of CD-associated NOD2/CARD15 mutations.
Highlights
Chronic inflammatory diseases where an external infectious or noxious agent is not readily identified as the direct cause of the associated pathology are usually categorized as autoimmune or immune-mediated conditions
This crucial difference between inflammatory bowel diseases (IBD) and other immunological conditions is at the core of the present review, and will allow us to consider the intriguing idea of the normal enteric flora not as an external environmental factor but an intrinsic, “self-component” of the intestine-specific immune response occurring in Crohn’s disease (CD) and ulcerative colitis (UC)
Serum antibodies against colonic epithelium were detected in the circulation of UC patients that were cross-reactive with Escherichia coli antigens, and the hypothesis was proposed that such immune cross-reactivity could represent a form of autoimmunity relevant to IBD pathogenesis (Perlmann et al, 1967)
Summary
Division of Gastroenterology, University Hospitals of Cleveland, Case Western Reserve University School of Medicine, Cleveland, OH 44106-4952, USA. The pathogenesis of Crohn’s disease (CD) and ulcerative colitis (UC), the two main forms of inflammatory bowel disease (IBD), is still unclear, but both autoimmune and immune-mediated phenomena are involved. Autoimmune phenomena include the presence of serum and mucosal autoantibodies against intestinal epithelial cells in either form of IBD, and against human tropomyosin fraction five selectively in UC. Various complementary factors probably contribute to the loss of tolerance to commensal bacteria in IBD. They include defects in regulatory T-cell function, excessive stimulation of mucosal dendritic cells, infections or variants of proteins critically involved in bacterial antigen recognition, such as the products of CD-associated NOD2/CARD15 mutations
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