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Expression data in CD4 T cells from lungs of PBS or house dust mite treated mice

ABSTRACT: CD4 T cells are essential mediators of the asthmatic process. We used the clinically relevant allergen house dust mites to induce signs of allergy in mice and performed gene expression arrays specifically on CD4 T cells infiltrating the lung Reference: IL-21-producing CD4+ T cells promote type 2 immunity to house dust mites

ORGANISM(S): Mus musculus

PROVIDER: GSE72005 | GEO | 2015/08/13

SECONDARY ACCESSION(S): PRJNA292704

REPOSITORIES: GEO

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Expression data in CD4 T cells from lungs of PBS or house dust mite treated mice

Project description:CD4 T cells are essential mediators of the asthmatic process. We used the clinically relevant allergen house dust mites to induce signs of allergy in mice and performed gene expression arrays specifically on CD4 T cells infiltrating the lung Reference: IL-21-producing CD4+ T cells promote type 2 immunity to house dust mites Primary CD4+ T cells were isolated from mice sensitised and challenged to either house dust mites or PBS. Purification of CD4 T cells was performed by flow cytometry. RNA was isolated, converted to cDNA and then hybridised on Affymetrix GeneChip Mouse Gene 2.0 ST Arrays

2015-08-13 | E-GEOD-72005 | biostudies-arrayexpress

Human airway epithelial cell response to LPS and house dust mite antigen

2009-10-01 | GSE8190 | GEO

Human airway inflammatory cell response to LPS and house dust mite antigen

2009-10-01 | GSE5272 | GEO

Transcription profiling of human airway epithelial cell response to LPS and house dust mite antigen

Project description:Allergic asthmatic, allergy only, asthma only (no allergy), and non-allergic non-asthmatic (control) subjects underwent bronchoscopy with instillation of saline, lipopolysaccharide (LPS), and house dust mite antigen in separate subsegmental bronchi. Airway epithelial cells were collected four hours later (three samples per subject). RNA was extracted from these cells for microarray analysis. Experiment Overall Design: There are four main phenotypic groups: Experiment Overall Design: 1. control (no allergy or asthma) Experiment Overall Design: 2. allergy only (no asthma) Experiment Overall Design: 3. asthma only (no allergy) Experiment Overall Design: 4. allergy and asthma Experiment Overall Design: and three exposures: saline, house dust mite antigen (HDM), and LPS. Samples from the different exposures were all collected at the same time: four hours after instillation. The hybridizations were carried out in two main "batches": samples in batch 1 were processed in mid 2004, samples in batch 2 about a year later in 2005. There is a clear "batch effect": differences between expression profiles from the two batches (likely caused by technical differences between hybridization and scanning methods). This should be considered when analyzing the data.

2009-10-11 | E-GEOD-8190 | biostudies-arrayexpress

Transcription profiling of human bronchoalveolar to investigate airway inflammatory cell response to lipopolysaccharide and house dust mite antigen

Project description:Allergic asthmatic, allergy only, asthma only (no allergy), and non-allergic non-asthmatic (control) subjects underwent bronchoscopy with instillation of saline, lipopolysaccharide (LPS), and house dust mite antigen in separate subsegmental bronchi. Bronchoalveolar lavage (BAL) fluid was collected four hours later (three samples per subject). Inflammatory cells from each specimen were isolated and RNA was extracted for microarray analysis. Experiment Overall Design: There are four main phenotypic groups: Experiment Overall Design: 1. control (no allergy or asthma) Experiment Overall Design: 2. allergy only (no asthma) Experiment Overall Design: 3. asthma only (no allergy) Experiment Overall Design: 4. allergy and asthma Experiment Overall Design: and three exposures: saline, house dust mite antigen (HDM), and LPS. Experiment Overall Design: Samples from the different exposures were all collected at the same time: four hours after instillation. The hybridizations were carried out in two main 'batches': samples in batch 1 were processed in mid 2004, samples in batch 2 about a year later in 2005. There is a clear 'batch effect': differences between expression profiles from the two batches (likely caused by technical differences between hybridization and scanning methods). This should be considered when analyzing the data.

2009-10-10 | E-GEOD-5272 | biostudies-arrayexpress

RNA-Seq analysis of BEAS-2b cells stimulated with house dust mite extract with or without suppression of MD-2

Project description:We clarified MD-2 might have a protective role in house dust mite(HDM)-induced asthmatic characteristics. The purpose of RNA-Seq analysis is to identify transcriptional events regulated by MD-2 in HDM-stimulated airway epithelial cells.

2020-09-23 | GSE158386 | GEO

Gene expression patterns in house dust mite stimulated CD4 T cells and IgG:IgE ratios

Project description:PBMC from house dust mite (HDM) sensitized atopics were cultured in the presence or absence of HDM extract for 24 hours. At the termination of the cultures, CD4 T cells were isolated using immunomagnetic separation. Gene expression was profiled on microarrays.

2015-11-03 | GSE70760 | GEO

Transcriptional changes in mouse lungs induced by house dust mite

Project description:We examined the transcriptional changes in mouse lungs induced by house dust mite (HDM), D.f. extract and the isolated RNA was utilized for RNA-seq analysis. Our results demonstrated that HDM strongly triggered an inflammatory response.

2019-08-01 | GSE102211 | GEO

Gene expression patterns in house dust mite stimulated CD4 T cells and IgG:IgE ratios

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Mouse skin CD45 cells in house dust mite dermatitis

Project description:Despite robust literature associating IL-31 with pruritic inflammatory skin diseases, its influence on cutaneous inflammation and on the interplay between inflammatory and neurosensory pathways remain unmapped. Here, we examined the consequences of disrupting Il31 and its receptor Il31ra in a mouse model of house dust mite (HDM) allergic dermatitis. Il31-deficient mice displayed an increased number and proportion of cutaneous type 2 cytokine-producing CD4 T cells and serum IgE in response to HDM. Single cell RNA-sequencing analysis of skin CD45+ populations from HDM-treated skin revealed that Il4ra+ monocytes and macrophages capable of fueling a feedforward type 2 inflammatory loop were selectively enriched in Il31ra-deficient HDM dermatitis skin. Thus, IL-31 is not strictly a pro-inflammatory cytokine, but rather an immunoregulatory factor that limits the magnitude of type 2 inflammatory responses in skin.

2023-10-26 | GSE236744 | GEO

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