Abstract

BackgroundAtopic dermatitis (AD) is a multifactorial chronic inflammatory skin disease presenting with a relapsing clinical pattern similar to chronic autoimmune disease. Several human transglutaminases have been defined and keratinocyte transglutaminase (TG1) and epidermal transglutaminase (TG3) expressed in the epidermis are associated with epidermal barrier dysfunction. Since impairments to the epidermal barrier represent an important factor in AD, we hypothesized that IgA autoantibodies specific for TG1 (IgA-anti-TG1) and TG3 (IgA-anti-TG3) may affect AD development during childhood.MethodsActive AD patients (n = 304), 28 patients with biopsy-confirmed coeliac disease (CD), 5 patients with active AD and CD, and 55 control patients without CD and skin diseases were enrolled into the study. IgA-anti-TG1 and IgA-anti-TG3 reactivity was determined using an enzyme-linked immunosorbent assay. IgA-anti-TG2 were defined using a fluoroenzyme immunoassay.ResultsIgA-anti-TG1 antibodies were found in 2% and IgA-anti-TG3 antibodies in 3% of patients with active AD. Two out of the 5 patients with AD and concomitant CD had IgA-anti-TG1 and IgA-anti-TG2 antibodies. In CD patients, 36% of individuals presented with elevated IgA-anti-TG1 antibodies and 18% presented with elevated IgA-anti-TG3 antibodies and all CD patients presented with IgA-anti-TG2 antibodies (significantly different from AD patients and controls, p < 0.05). In CD patients, IgA-anti-TG1 and/or IgA-anti-TG3 seropositivity tended to appear concurrently, whereas only one patient with AD had both types of autoantibodies.ConclusionsIgA-anti-TG1 and IgA-anti-TG3 seropositivity was rare in active AD but frequent in CD patients. The level of circulating antibodies related to skin lesions could be studied by determining the levels of IgA-anti-TG1 and IgA-anti-TG3 in skin biopsies of AD patients.

Highlights

  • Atopic dermatitis (AD) is a multifactorial chronic inflammatory skin disease presenting with a relapsing clinical pattern similar to chronic autoimmune disease

  • No patients in the AD group presented with IgA-anti-TG2 and 7 patients (2%) had slight IgAanti-deamidated gliadin peptides (DGP) reactivity

  • Elevated IgA-anti-DGP values were found in the sera of 2 control group patients, both

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Summary

Introduction

Atopic dermatitis (AD) is a multifactorial chronic inflammatory skin disease presenting with a relapsing clinical pattern similar to chronic autoimmune disease. Keratinocyte transglutaminase (TG1) and epidermal transglutaminase (TG3) are expressed in the spinous and granular layers of the epidermis [10], while tissue transglutaminase (TG2) is widely expressed in various tissues, including the gut epithelium. Their expression in the epidermis can be demonstrated only under specific conditions [10,11]. Despite the diagnostic sensitivity of IgA-anti-TG2 for CD, children < 24 months of age have been shown to have a decreased ability to produce antibodies to TG2 [13] Instead, these patients may have antibodies against deamidated gliadin peptides (DGP), another type of autoantibody associated with CD. Mutations in the TG1 coding gene have been reported to be deficient in lamellar ichthyosis, a disease with severely impaired epidermal barriers [10]

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