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Gene expression analysis in canine discoid/chronic lupus erythematosus, mucocutaneous lupus erythematosus and pyoderma

ABSTRACT: Gene expression analysis in canine discoid/chronic lupus erythematosus, mucocutaneous lupus erythematosus and pyoderma

PROVIDER: PRJNA672714 | ENA |

REPOSITORIES: ENA

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Gene expression analysis in canine discoid/chronic lupus erythematosus, mucocutaneous lupus erythematosus and pyoderma

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Gene expression in cutaneous lupus erythematosus

Project description:Lesional skin biopsies were taken from patients with active, untreated lupus skin disease (chronic discoid lupus erythematosus, CDLE, n=6; subacute cutaneous lupus erythematosus, SCLE, n=5). Healthy control specimens (HC) were obtained from healthy skin of 5 patients undergoing plastic surgery. In every case, two 4mm punch biopsies were taken. One was flash-frozen in liquid nitrogen and afterwards processed for mRNA isolation. The second biopsy was fixed in 5% formalin solution overnight, and was proceeded for histological investigation.The one-color Agilent 60-mer oligo microarray (Agilent, Santa Clara, CA) was used for gene expression analyses. Statistical analyses were performed using the Agilent Feature Extraction Softwareâ¢ and the Rosetta Resolverâ¢ gene expression data analysis system. The presented gene list (Table S1) includes normalized sample/ control log10-ratios (expression > 2-fold enhanced, p<0.01).

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Plucked hair follicles from patients with chronic discoid lupus erythematosus show a disease-specific molecular signature

Project description:When faced with clinical symptoms of scarring alopecia – the standard diagnostic pathway involves a scalp biopsy which is an invasive and expensive procedure. Furthermore, clinical activity of scarring alopecias is often difficult to assess as symptoms of permanent damage and signs of activity can overlap or be difficult to distinguish. Here we report that gene expression analysis of only a small number of hair follicles (HF) plucked from lesional areas of the scalp is sufficient to characterise chronic discoid lupus erythematosus (CDLE). Lesional and non-lesional HFs were extracted from the scalp of patients with CDLE, psoriasis and healthy controls. The expression profile from CDLE HFs coincides with published profiles of CDLE from skin biopsy and was consistent with histopathological diagnostic features of CDLE. We therefore propose that information obtained from this non-invasive approach are sufficient to diagnose scalp LE.

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Project description:Cutaneous lupus erythematosus (CLE) is a disfiguring disease that can exist as an independent entity or as a manifestation of systemic lupus erythematosus (SLE) where up to 70% of patients experience lesions during their disease course. Subacute CLE (sCLE) is an inflammatory lesion with associated erythema in papulosquamous or annular formations. Typically, sCLE does not scar but depigmentation can occur. Importantly, sCLE is associated with a higher progression to SLE. Discoid lesions (DLE) are often circular and frequently lead to alopecia and scar formation. sCLE lesions have a higher propensity for photoprovocation and a more robust inflammatory infiltrate following ultraviolet (UV) B exposure. The pathogenic mechanisms which govern the differences between DLE and sCLE remain poorly defined, and this is reflected by the refractory nature of cutaneous lesions to usual lupus therapies. In this study, we evaluated the transcriptional profiles of 26 DLE and 23 sCLE biopsies and compared them to control skin and to each other in order to develop a comprehensive understanding of the similarities and differences between these two clinical subtypes.

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Project description:Discoid lupus erythematosus (DLE) is the most common skin manifestation of lupus. Despite its high frequency in systemic lupus in addition to cases without extracutaneous manifestations, targeted treatments for DLE are lacking, likely because of a dearth of knowledge of the molecular landscape of DLE skin. Here, we profiled the transcriptome of DLE skin in order to identify signaling pathways and cellular signatures that may be targeted for treatment purposes. Further comparison of the DLE transcriptome with that of psoriasis, a useful reference given our extensive knowledge of molecular pathways in this disease, provided a framework to identify potential therapeutic targets. Although a growing body of data support a role for IL-17 and T helper type 17 (Th17) cells in systemic lupus, we show a relative enrichment of IFN-Œ≥-associated genes without that for IL-17-associated genes in DLE. Extraction of T cells from the skin of DLE patients identified a predominance of IFN-Œ≥-producing Th1 cells and an absence of IL-17-producing Th17 cells, complementing the results from whole-skin transcriptomic analyses. These data therefore support investigations into treatments for DLE that target Th1 cells or the IFN-Œ≥ signaling pathway. Comparison of transcriptomes between skin conditions

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Project description:Discoid lupus erythematosus (DLE) is the most common skin manifestation of lupus. Despite its high frequency in systemic lupus in addition to cases without extracutaneous manifestations, targeted treatments for DLE are lacking, likely because of a dearth of knowledge of the molecular landscape of DLE skin. Here, we profiled the transcriptome of DLE skin in order to identify signaling pathways and cellular signatures that may be targeted for treatment purposes. Further comparison of the DLE transcriptome with that of psoriasis, a useful reference given our extensive knowledge of molecular pathways in this disease, provided a framework to identify potential therapeutic targets. Although a growing body of data support a role for IL-17 and T helper type 17 (Th17) cells in systemic lupus, we show a relative enrichment of IFN-γ-associated genes without that for IL-17-associated genes in DLE. Extraction of T cells from the skin of DLE patients identified a predominance of IFN-γ-producing Th1 cells and an absence of IL-17-producing Th17 cells, complementing the results from whole-skin transcriptomic analyses. These data therefore support investigations into treatments for DLE that target Th1 cells or the IFN-γ signaling pathway.

2013-11-18 | GSE52471 | GEO

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