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Gene Expression Profiling in Dermatitis Herpetiformis Skin Lesions
Dermatitis herpetiformis (DH) is an autoimmune blistering skin disease associated with gluten-sensitive enteropathy (CD). In order to investigate the pathogenesis of skin lesions at molecular level, we analysed the gene expression profiles in skin biopsies from 6 CD patients with DH and 6 healthy co...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3443590/ https://www.ncbi.nlm.nih.gov/pubmed/22991566 http://dx.doi.org/10.1155/2012/198956 |
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author | Dolcino, M. Cozzani, E. Riva, S. Parodi, A. Tinazzi, E. Lunardi, C. Puccetti, A. |
author_facet | Dolcino, M. Cozzani, E. Riva, S. Parodi, A. Tinazzi, E. Lunardi, C. Puccetti, A. |
author_sort | Dolcino, M. |
collection | PubMed |
description | Dermatitis herpetiformis (DH) is an autoimmune blistering skin disease associated with gluten-sensitive enteropathy (CD). In order to investigate the pathogenesis of skin lesions at molecular level, we analysed the gene expression profiles in skin biopsies from 6 CD patients with DH and 6 healthy controls using Affymetrix HG-U133A 2.0 arrays. 486 genes were differentially expressed in DH skin compared to normal skin: 225 were upregulated and 261 were downregulated. Consistently with the autoimmune origin of DH, functional classification of the differentially expressed genes (DEGs) indicates a B- and T-cell immune response (LAG3, TRAF5, DPP4, and NT5E). In addition, gene modulation provides evidence for a local inflammatory response (IL8, PTGFR, FSTL1, IFI16, BDKRD2, and NAMPT) with concomitant leukocyte recruitment (CCL5, ENPP2), endothelial cell activation, and neutrophil extravasation (SELL, SELE). DEGs also indicate overproduction of matrix proteases (MMP9, ADAM9, and ADAM19) and proteolytic enzymes (CTSG, ELA2, CPA3, TPSB2, and CMA1) that may contribute to epidermal splitting and blister formation. Finally, we observed modulation of genes involved in cell growth inhibition (CGREF1, PA2G4, and PPP2R1B), increased apoptosis (FAS, TNFSF10, and BASP1), and reduced adhesion at the dermal epidermal junction (PLEC1, ITGB4, and LAMA5). In conclusion, our results identify genes that are involved in the pathogenesis of DH skin lesions. |
format | Online Article Text |
id | pubmed-3443590 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-34435902012-09-18 Gene Expression Profiling in Dermatitis Herpetiformis Skin Lesions Dolcino, M. Cozzani, E. Riva, S. Parodi, A. Tinazzi, E. Lunardi, C. Puccetti, A. Clin Dev Immunol Research Article Dermatitis herpetiformis (DH) is an autoimmune blistering skin disease associated with gluten-sensitive enteropathy (CD). In order to investigate the pathogenesis of skin lesions at molecular level, we analysed the gene expression profiles in skin biopsies from 6 CD patients with DH and 6 healthy controls using Affymetrix HG-U133A 2.0 arrays. 486 genes were differentially expressed in DH skin compared to normal skin: 225 were upregulated and 261 were downregulated. Consistently with the autoimmune origin of DH, functional classification of the differentially expressed genes (DEGs) indicates a B- and T-cell immune response (LAG3, TRAF5, DPP4, and NT5E). In addition, gene modulation provides evidence for a local inflammatory response (IL8, PTGFR, FSTL1, IFI16, BDKRD2, and NAMPT) with concomitant leukocyte recruitment (CCL5, ENPP2), endothelial cell activation, and neutrophil extravasation (SELL, SELE). DEGs also indicate overproduction of matrix proteases (MMP9, ADAM9, and ADAM19) and proteolytic enzymes (CTSG, ELA2, CPA3, TPSB2, and CMA1) that may contribute to epidermal splitting and blister formation. Finally, we observed modulation of genes involved in cell growth inhibition (CGREF1, PA2G4, and PPP2R1B), increased apoptosis (FAS, TNFSF10, and BASP1), and reduced adhesion at the dermal epidermal junction (PLEC1, ITGB4, and LAMA5). In conclusion, our results identify genes that are involved in the pathogenesis of DH skin lesions. Hindawi Publishing Corporation 2012 2012-09-06 /pmc/articles/PMC3443590/ /pubmed/22991566 http://dx.doi.org/10.1155/2012/198956 Text en Copyright © 2012 M. Dolcino et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Dolcino, M. Cozzani, E. Riva, S. Parodi, A. Tinazzi, E. Lunardi, C. Puccetti, A. Gene Expression Profiling in Dermatitis Herpetiformis Skin Lesions |
title | Gene Expression Profiling in Dermatitis Herpetiformis Skin Lesions |
title_full | Gene Expression Profiling in Dermatitis Herpetiformis Skin Lesions |
title_fullStr | Gene Expression Profiling in Dermatitis Herpetiformis Skin Lesions |
title_full_unstemmed | Gene Expression Profiling in Dermatitis Herpetiformis Skin Lesions |
title_short | Gene Expression Profiling in Dermatitis Herpetiformis Skin Lesions |
title_sort | gene expression profiling in dermatitis herpetiformis skin lesions |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3443590/ https://www.ncbi.nlm.nih.gov/pubmed/22991566 http://dx.doi.org/10.1155/2012/198956 |
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