Risk of Morbidity in Contemporary Celiac Disease

Nina R Lewis; Geoffrey KT Holmes


Expert Rev Gastroenterol Hepatol. 2010;4(6):767-780. 

In This Article

Are Celiac Pathogenic Factors Implicated in the Morbidity?

The mechanisms of the intestinal immune-mediated response in celiac disease are not completely clear, but the pathogenesis is thought to involve a complex interplay of immunological factors including tissue transglutaminase, intraepithelial lymphocytes, cytotoxic T cells, adaptive and innate immune responses and autoimmunity.[14] Such pathogenic factors may predispose celiacs to developing other conditions. Autoantibodies directed against tissue transglutaminase are present in the liver and other extraintestinal tissues such as the thyroid in celiac disease, raising the possibility of a pathogenic role for the humoral-mediated immune responses in the hepatocyte and thyroid injuries observed.[15,16] Increased intestinal permeability resulting from the intestinal immune-mediated response to gluten may facilitate the entrance of toxins, antigens and proinflammatory mediators such as interleukins and IFN-γ into the circulation, with subsequent tissue insult that may be of importance in provoking autoimmune disorders and lymphoma.[17] There may be a shared immunogenetic susceptibility to developing immune dysregulation.[18] For example, IDDM1, a candidate allelic locus identified for Type 1 diabetes that is located on chromosome 6q21, is found at the exact same position as loci for celiac disease (marker HLA-DQ2),[19] Crohn's disease[20] and lupus.[21] Monoclonal intraepithelial lymphocytes are implicated in the development of enteropathy-associated T-cell lymphoma and ulcerative jejunitis.[22]


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