Dermatitis herpetiformis (DH) is an autoimmune blistering skin disorder that is 
associated with gluten sensitivity. It presents as a papulovesicular rash and is 
often associated with enteropathy. The rash resolves when the patient is placed 
on a gluten-free diet and/or dapsone. DH, as well as celiac disease, is tightly 
associated with DQ2 and DQ8. A novel mouse model for DH is described that 
utilizes the NOD background and the HLA-DQ8 transgene. The addition of DQ8 
contributes sensitivity to gliadin, and the addition of the NOD background 
contributes to autoimmunity and pathogenesis. Fifteen NOD DQ8+ mice of 90 that 
were sensitized to gluten developed blistering pathology similar to that seen in 
DH. Neutrophil infiltration of the dermis, deposition of IgA at the 
dermal-epidermal junction, and a complete reversal of the blistering phenomenon 
with the administration of a gluten-free diet with or without dapsone were 
observed. None of the 3 blistering mice examined had small-bowel pathology. This 
animal model of DH will be useful to determine the specificity of the IgA 
deposits, as well as the pathogenic mechanisms that occur in the skin as a 
result of gluten ingestion.