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Epidermal Transglutaminase (TGase 3) Is the Autoantigen of Dermatitis Herpetiformis
Gluten sensitivity typically presents as celiac disease, a common chronic small intestinal disorder. However, in certain individuals it is associated with dermatitis herpetiformis, a blistering skin disease characterized by granular IgA deposits in the papillary dermis. While tissue transglutaminase...
Autores principales: | , , , , |
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
2002
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193738/ https://www.ncbi.nlm.nih.gov/pubmed/11901200 http://dx.doi.org/10.1084/jem.20011299 |
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author | Sárdy, Miklós Kárpáti, Sarolta Merkl, Barbara Paulsson, Mats Smyth, Neil |
author_facet | Sárdy, Miklós Kárpáti, Sarolta Merkl, Barbara Paulsson, Mats Smyth, Neil |
author_sort | Sárdy, Miklós |
collection | PubMed |
description | Gluten sensitivity typically presents as celiac disease, a common chronic small intestinal disorder. However, in certain individuals it is associated with dermatitis herpetiformis, a blistering skin disease characterized by granular IgA deposits in the papillary dermis. While tissue transglutaminase has been implicated as the major autoantigen of gluten sensitive disease, there has been no explanation as to why this condition appears in two distinct forms. Here we show that while sera from patients with either form of gluten sensitive disease react both with tissue transglutaminase and the related enzyme epidermal (type 3) transglutaminase, antibodies in patients having dermatitis herpetiformis show a markedly higher avidity for epidermal transglutaminase. Further, these patients have an antibody population specific for this enzyme. We also show that the IgA precipitates in the papillary dermis of patients with dermatitis herpetiformis, the defining signs of the disease, contain epidermal transglutaminase, but not tissue transglutaminase or keratinocyte transglutaminase. These findings demonstrate that epidermal transglutaminase, rather than tissue transglutaminase, is the dominant autoantigen in dermatitis herpetiformis and explain why skin symptoms appear in a proportion of patients having gluten sensitive disease. |
format | Text |
id | pubmed-2193738 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2002 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21937382008-04-14 Epidermal Transglutaminase (TGase 3) Is the Autoantigen of Dermatitis Herpetiformis Sárdy, Miklós Kárpáti, Sarolta Merkl, Barbara Paulsson, Mats Smyth, Neil J Exp Med Original Article Gluten sensitivity typically presents as celiac disease, a common chronic small intestinal disorder. However, in certain individuals it is associated with dermatitis herpetiformis, a blistering skin disease characterized by granular IgA deposits in the papillary dermis. While tissue transglutaminase has been implicated as the major autoantigen of gluten sensitive disease, there has been no explanation as to why this condition appears in two distinct forms. Here we show that while sera from patients with either form of gluten sensitive disease react both with tissue transglutaminase and the related enzyme epidermal (type 3) transglutaminase, antibodies in patients having dermatitis herpetiformis show a markedly higher avidity for epidermal transglutaminase. Further, these patients have an antibody population specific for this enzyme. We also show that the IgA precipitates in the papillary dermis of patients with dermatitis herpetiformis, the defining signs of the disease, contain epidermal transglutaminase, but not tissue transglutaminase or keratinocyte transglutaminase. These findings demonstrate that epidermal transglutaminase, rather than tissue transglutaminase, is the dominant autoantigen in dermatitis herpetiformis and explain why skin symptoms appear in a proportion of patients having gluten sensitive disease. The Rockefeller University Press 2002-03-18 /pmc/articles/PMC2193738/ /pubmed/11901200 http://dx.doi.org/10.1084/jem.20011299 Text en Copyright © 2002, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Original Article Sárdy, Miklós Kárpáti, Sarolta Merkl, Barbara Paulsson, Mats Smyth, Neil Epidermal Transglutaminase (TGase 3) Is the Autoantigen of Dermatitis Herpetiformis |
title | Epidermal Transglutaminase (TGase 3) Is the Autoantigen of Dermatitis Herpetiformis |
title_full | Epidermal Transglutaminase (TGase 3) Is the Autoantigen of Dermatitis Herpetiformis |
title_fullStr | Epidermal Transglutaminase (TGase 3) Is the Autoantigen of Dermatitis Herpetiformis |
title_full_unstemmed | Epidermal Transglutaminase (TGase 3) Is the Autoantigen of Dermatitis Herpetiformis |
title_short | Epidermal Transglutaminase (TGase 3) Is the Autoantigen of Dermatitis Herpetiformis |
title_sort | epidermal transglutaminase (tgase 3) is the autoantigen of dermatitis herpetiformis |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193738/ https://www.ncbi.nlm.nih.gov/pubmed/11901200 http://dx.doi.org/10.1084/jem.20011299 |
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