Autoantibodies against epidermal transglutaminase are a sensitive diagnostic marker in patients with dermatitis herpetiformis on a normal or gluten-free diet

Rosé, Christian; Armbruster, Franz Paul; Ruppert, Jana; Igl, Bernd‐Wolfgang; Zillikens, Detlef; Shimanovich, Iakov

doi:10.1016/j.jaad.2008.12.037

Cited by 88 publications

(66 citation statements)

References 16 publications

(19 reference statements)

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“…Although DH patients may present with longterm severe intestinal disease, they tend to have a generally less severe form of celiac disease and tend to be diagnosed at a later age than celiac patients (24). IgA TG2 Abs are present in most DH patients (10,25,26). TG3 is also produced in the gut.…”

Section: Discussionmentioning

confidence: 99%

Dermatitis Herpetiformis Sera or Goat Anti–Transglutaminase-3 Transferred to Human Skin-Grafted Mice Mimics Dermatitis Herpetiformis Immunopathology

Zone

Schmidt

Taylor

et al. 2011

The Journal of Immunology

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Dermatitis herpetiformis (DH) is characterized by deposition of IgA in the papillary dermis. However, indirect immunofluorescence is routinely negative, raising the question of the mechanism of formation of these immune deposits. Sárdy et al. (2002. J. Exp. Med. 195: 747–757) reported that transglutaminase-3 (TG3) colocalizes with the IgA. We sought to create such deposits using passive transfer of Ab to SCID mice bearing human skin grafts. IgG fraction of goat anti-TG3 or control IgG were administered i.p. to 20 mice. Separately, sera from seven DH patients and seven controls were injected intradermally. Biopsies were removed and processed for routine histology as well as direct immunofluorescence. All mice that received goat anti-TG3 produced papillary dermal immune deposits, and these deposits reacted with both rabbit anti-TG3 and DH patient sera. Three DH sera high in IgA anti-TG3 also produced deposits of granular IgA and TG3. We hypothesize that the IgA class anti-TG3 Abs are directly responsible for the immune deposits and that the TG3 is from human epidermis, as this is its only source in our model. These deposits seem to form over weeks in a process similar to an Ouchterlony immunodiffusion precipitate. This process of deposition explains the negative indirect immunofluorescence results with DH serum.

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Section: Discussionmentioning

confidence: 99%

Dermatitis Herpetiformis Sera or Goat Anti–Transglutaminase-3 Transferred to Human Skin-Grafted Mice Mimics Dermatitis Herpetiformis Immunopathology

Zone

Schmidt

Taylor

et al. 2011

The Journal of Immunology

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“…Doku ve epidermal transglutaminaza karşı oluşmuş IgA'yı saptamak amacıyla geliştirilmiş sensitif (sırasıyla; %47-95, %52-100) ve spesifik (her ikisi de >%90) ticari ELISA sistemleri mevcuttur (60,61). Anti-DPG (sentetik gliadin derive peptid) antikorlarına ise (sensitivitesi; %55 IgA, %50 IgG) şüpheli durumlarda bakılması önerilmektedir.…”

Section: Dermatitis Herpetiformisunclassified

Serological Diagnosis of Autoimmune Blistering Diseases

Özkesici¹,

Karakaş²

2016

tdd

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“…63 Moreover, serum TG3-targeted autoantibodies are found in patients with dermatitis herpetiformis, and they seem to be gluten dependent. 64,65 Celiac disease may also present with neurological complications, such as dementia, brain atrophy, cerebellar ataxia, peripheral neuropathy and epilepsy with occipital calcifications. 6 Gluten ataxia is a sporadic cerebellar ataxia associated with the presence of AGA without other apparent etiologies for the ataxia.…”

Section: Intestinal Autoantibodiesmentioning

confidence: 99%