Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA94945 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Glucocorticoid responsive AIED patients demonstrate alternate splicing of IL1R2 in response to dexamethasone prior to treatment. Identification of IL1R2 as a potential target gene in AIED was determined by a microarray analysis of patients with end-stage AIED and controls with non-immunologic etiologies of hearing loss undergoing cochlear implantation.
2009-04-29 | GSE4277 | GEO
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2019-07-31 | GSE114179 | GEO
Project description:Glucocorticoid responsive AIED patients demonstrate alternate splicing of IL1R2 in response to dexamethasone prior to treatment. Identification of IL1R2 as a potential target gene in AIED was determined by a microarray analysis of patients with end-stage AIED and controls with non-immunologic etiologies of hearing loss undergoing cochlear implantation. Experiment Overall Design: Patients with either end-stage AIED or controls with non-immunologic etiologies of hearing loss undergoing cochlear implantation were enrolled. All patients received pneumovax 2 weeks prior to surgery. At the time of surgery, blood was taken for PBMC isolation and autologous perilymph was harvested from a bloodless field. For each patient, 3 microarrays were performed: (1) unstimulated PBMC, (2) pneumovax stimulated PBMC, (3) autologous perilymph stimulated PBMC. All conditions were compared for the AIED and control subjects. IL1R2 was identified as induced in controls, but not AIED patients, in response to autologous perilymph. Findings were confirmed by QPCR.
2009-05-11 | E-GEOD-4277 | biostudies-arrayexpress
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Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO
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Project description:Transcriptional profiling of Homo sapiens inflammatory skin diseases (whole skin biospies): Psoriasis (Pso), vs Atopic Dermatitis (AD) vs Lichen planus (Li), vs Contact Eczema (KE), vs Healthy control (KO) In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide. However, most of these markers are not psoriasis-specific but also found in other inflammatory disorders. We performed an unsupervised cluster analysis of gene expression profiles in 150 psoriasis patients and other inflammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls). We identified a cluster of IL-17/TNFα-associated genes specifically expressed in psoriasis, among which IL-36γ was the most outstanding marker. In subsequent immunohistological analyses IL-36γ was confirmed to be expressed in psoriasis lesions only. IL-36γ peripheral blood serum levels were found to be closely associated with disease activity, and they decreased after anti-TNFα-treatment. Furthermore, IL-36γ immunohistochemistry was found to be a helpful marker in the histological differential diagnosis between psoriasis and eczema in diagnostically challenging cases. These features highlight IL-36γ as a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course. Furthermore, IL-36γ might also provide a future drug target, due to its potential amplifier role in TNFα- and IL-17 pathways in psoriatic skin inflammation. In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide. However, most of these markers are not psoriasis-specific but also found in other inflammatory disorders. We performed an unsupervised cluster analysis of gene expression profiles in 150 psoriasis patients and other inflammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls). We identified a cluster of IL-17/TNFα-associated genes specifically expressed in psoriasis, among which IL-36γ was the most outstanding marker. In subsequent immunohistological analyses IL-36γ was confirmed to be expressed in psoriasis lesions only. IL-36γ peripheral blood serum levels were found to be closely associated with disease activity, and they decreased after anti-TNFα-treatment. Furthermore, IL-36γ immunohistochemistry was found to be a helpful marker in the histological differential diagnosis between psoriasis and eczema in diagnostically challenging cases. These features highlight IL-36γ as a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course. Furthermore, IL-36γ might also provide a future drug target, due to its potential amplifier role in TNFα- and IL-17 pathways in psoriatic skin inflammation.
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