Abstract
Dermatitis herpetiformis (DH) is caused by the consumption of gluten, which is also the trigger for celiac disease. DH is currently considered to be the skin manifestation of celiac disease, as both diseases have some degree of gluten-sensitive enteropathy. The human leukocyte antigens class II genes, DQ2 and DQ8, are tightly associated with both diseases, and there is an increased level of anti-gliadin antibodies in both diseases. Animal models of gluten sensitivity have been used to better understand the pathogenesis of both diseases. This paper describes these different models and discusses how certain elements of these models contribute to the development of DH.
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