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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...

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Autores principales: Dolcino, M., Cozzani, E., Riva, S., Parodi, A., Tinazzi, E., Lunardi, C., Puccetti, A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
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.
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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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