<p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p> <p>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 <italic>Saccharomyces
             cerevisiae</italic> (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
               <italic>NOD2/CARD15</italic> mutations.</p>
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Clin Dev Immunol. 2004 Sep-Dec; 11(3-4):195-204