Regulatory T cells as well as IL-10 are reduced in the skin of patients with dermatitis herpetiformis

• Tregs and IL-10 are reduced in the skin of patients with dermatitis herpetiformis (DH).
• Reduction of Tregs may lead to a defective suppressive function in DH lesions.
• No difference in Tregs can be found in the duodenum and blood of patients with DH and celiac disease.

BackgroundDermatitis herpetiformis (DH) and celiac disease (CD) are considered as autoimmune diseases that share a defined trigger (gluten) and a common genetic background (HLA-DQ2/DQ8). However, the pathogenesis of DH is not fully understood and no data are available about the immune regulation in such a disease.ObjectiveThe aim of this study was to assess if alterations in the pattern of the immune response and, in particular, impairments of regulatory T (Tregs) cells may contribute to the phenotypic differences between DH and CD.MethodsWe investigated the presence of Tregs cell markers, in the skin, the duodenum and the blood of patients with DH by immunohistochemistry, confocal microscopy and flow cytometry. As controls, we included patients with bullous pemphigoid, patients with CD without skin lesions, as well as healthy subjects (HS).ResultsIn the skin of DH patient, we found a significantly lower proportion of FOXP3+ Tregs and IL-10+ cells than in HS (p < 0.001 for both cell populations). In duodenal samples, no differences where found in the proportion of Tregs between patients with DH and patients with CD without skin manifestations. Finally, the frequency of CD25brightFOXP3+ cells within the CD4+ subset was significantly reduced in CD patients either with or without DH with respect to HS (p = 0.029 and p = 0.017, respectively).ConclusionsOur findings suggested that a reduction of Tregs may play a major role in the skin, leading to a defective suppressive function and thus to the development of the lesions. By contrast, no differences could be detected about Tregs between patients with DH and patients with CD in the duodenum, suggesting that the mechanisms of the intestinal damage are similar in both diseases.