Transglutaminases as diagnostically relevant autoantigens in patients with gluten sensitivity

Heil, P.; Volc‐Platzer, Beatrix; Karlhofer, Franz; Gebhart, W.; Huber, Wolf‐Dietrich; Benesch, Thomas; Vogelsang, Harald; Stingl, Georg

doi:10.1111/j.1610-0387.2005.05762.x

Cited by 13 publications

(1 citation statement)

References 21 publications

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“…A study by Rose et al [53] demonstrated that antibodies to eTG are the most sensitive serologic marker for the diagnosis of DH. In particular, a sensitivity of 95% was reported, confirming the study by Sardy et al [56], in which the sensitivity was 92%, although Heil et al [61] and Hull et al [62] found anti-eTG antibodies in only 45% and 52% of patients with untreated DH, respectively. …”

Section: Antitransglutaminase Iga Antibodiessupporting

confidence: 80%

Dermatitis Herpetiformis: From the Genetics to the Development of Skin Lesions

Bonciani

Verdelli

Bonciolini

et al. 2012

Clinical and Developmental Immunology

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Dermatitis herpetiformis (DH) is a rare autoimmune disease linked to gluten sensitivity with a chronic-relapsing course. It is currently considered to be the specific cutaneous manifestation of celiac disease (CD). Both conditions are mediated by the IgA class of autoantibodies, and the diagnosis of DH is dependent on the detection of granular deposits of IgA in the skin. There is an underlying genetic predisposition to the development of DH, but environmental factors are also important. This paper describes these different factors and discusses the known mechanism that lead to the development of skin lesions.

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Section: Antitransglutaminase Iga Antibodiessupporting

confidence: 80%

Dermatitis Herpetiformis: From the Genetics to the Development of Skin Lesions

Bonciani

Verdelli

Bonciolini

et al. 2012

Clinical and Developmental Immunology

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Transglutaminase 2 and Transglutaminase 2 Autoantibodies in Celiac Disease: a Review

Rauhavirta

Hietikko

Salmi

et al. 2016

Clinic Rev Allerg Immunol

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Celiac disease is a common inflammatory disorder with a prevalence of 1-2 % in which a distinct dietary wheat, rye, and barley component, gluten, induces small-bowel mucosal villous atrophy, crypt hyperplasia, and inflammation. The small-bowel mucosal damage can be reversed by a strict lifelong gluten-free diet, which is currently the only effective treatment for the condition. A key player in the pathogenetic process leading to the enteropathy is played by a protein called transglutaminase 2 (TG2), which is able to enzymatically modify gluten-derived gliadin peptides. The TG2-catalyzed deamidation of the gliadin peptides results in their increased binding affinity to the disease-predisposing human leukocyte antigen (HLA) DQ2 and DQ8 molecules, thus enabling a strong immune response to be launched. Blocking the enzymatic activity of TG2 has thus been suggested as a suitable novel pharmacological approach to treat celiac disease. By virtue of its transamidation capacity, TG2 is also able to cross-link gliadin peptides to itself, this resulting in the generation of TG2-gliadin peptide complexes whose presence might provide an explanation for the generation of the TG2 autoantibodies characteristic of celiac disease. Due to their excellent specificity for the disorder, the TG2-targeted autoantibodies are widely used in the diagnostics as a first-line test to select patients for gastrointestinal endoscopy. More recently, it has come to be appreciated that these autoantibodies and also the TG2-specific B cells might play an active role in the disease pathogenesis. In this review, we assess the role of TG2, TG2-specific B cells, and autoantibodies in celiac disease.

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