Original papers
IgA autoantibodies to gliadin nonapeptides, tissue transglutaminase and epidermal transglutaminase are associated, but unrelated to neutrophil elastase expression in lesional skin in human dermatitis herpetiformis

Introduction: In dermatitis herpetiformis (DH), activation of neutrophils via IgA Fc receptors (e.g. CD89) and immunocomplexes containing IgA1 may lead to the release of proteolytic enzymes, mainly neutrophil elastase (NE), destruction of the dermal-epidermal junction and blister formation.

Aim: To analyze whether there are associations between levels of circulating IgA autoantibodies to epidermal (eTG) and tissue (tTG) transglutaminases, nonapeptides of gliadin (npG) and the intensity of cutaneous NE expression in patients with DH.

Material and methods: Altogether, 31 patients with DH were studied. The levels of serum IgA autoantibodies to eTG, tTG and npG were evaluated with ELISAs. The intensity of NE expression was estimated with immunohistochemistry using NE monoclonal antibody and quantitative digital morphometry. Statistical analysis was done using Spearman’s rank correlation coefficient.

Results: There were no statistically significant correlations between the intensity of cutaneous NE expression and the levels of serum IgA autoantibodies to eTG, tTG, npG in patients with DH. There were statistically significant correlations between the levels of IgA autoantibodies to eTG, tTG, npG.

Conclusions: It seems that in human DH the activation of neutrophils, judged by the NE expression, is unrelated to the levels of serum IgA autoantibodies to eTG/tTG/npG, but all those autoantibodies in DH are produced in a coordinated way.