Unknown,Transcriptomics,Genomics,Proteomics

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MicroRNA profiling of in vitro grass pollen extract (allergen) challenged CD4+T-cells against paired unchallenged controls from Seasonal Allergic Rhinitis patients

ABSTRACT: Differentiation of CD4+T-cells into effector subsets is a critical component of the adaptive immune system and an incorrect response can lead to autoimmunity or immune deficiency. Cellular differentiation including T-cell differentiation is accompanied by large-scale transcriptional changes, including expression of microRNAs involved in suppressing mRNA expression. We combined time-series microRNA and mRNA expression to construct a CD4+T-cell microRNA/mRNA regulatory network and identified 25 subnetworks (modules) which were associated with multiple T-cell related diseases. This dataset was designed to validate the disease association of the constructed microRNA/mRNA regulatory network and identified modules. Matching mRNA expression profiling was originally submitted to NCBI Gene Expression Omnibus and has been imported into ArrayExpress under accession E-GEOD-60677.

INSTRUMENT(S): Agilent G2565CA

ORGANISM(S): Homo sapiens

SUBMITTER: Antonio Lentini

PROVIDER: E-MTAB-4900 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Medical research focuses on disease-specific genes. By contrast, here we systematically examined the roles of shared genes for disease susceptibility and as therapeutic and diagnostic targets. Meta-analysis of all published disease-related genome-wide association studies (GWAS) showed that T helper (Th) cell differentiation was the most shared pathway. Expression profiling data from highly diverse CD4+ T cell-associated diseases revealed shared disease-associated genes, which were enriched for Th cell differentiation, but also metabolic and proliferative pathways. This pleiotropy suggested that altered functions of shared genes could generally increase disease susceptibility. Indeed, compared to specific genes, the shared genes were enriched for disease-associated SNPs identified by allÂ published disease-related GWAS. To examine if the shared genes induced disease-relevant pathways, we focused on transcription factors (TFs) that induced Th differentiation. Those TFs were enriched among the shared genes, as well as for disease-associated SNPs identified by GWAS, and disease-phenotypes in mice knock-out studies. Original GWAS and profiling data fromÂ patients with multiple sclerosis and allergyÂ confirmed enrichment of disease-associated SNPs in the TFs, and that the TFs were differentially expressed at early disease stages, and their targets increased in parallel with disease development. From a clinical perspective, the shared genes were significantly enriched for known diagnostic and therapeutic targets. Prospective clinical studies of multiple sclerosis and allergy showed that shared or specific genes could be used to stratify patients for individualized medicine. Our findings show that shared disease genes generally increase disease susceptibility and are important therapeutic and diagnostic targets. Patients with seasonal allergic rhinitis (SAR) show considerable variations in response to glucocorticoids (GCs) treatment. Peripheral blood mononuclear cells (PBMCs) were collected from 8 high responders (HR) and 8 low responders (LR) to GC treatment. PBMCs were challenged with diluent, grass pollen extract (ALK-AbellÃ³ A/S; 100 Î¼g/mL) as well as grass pollen extract plus glucocorticoids (100ug/mL) for one week. Total CD4+ T cells were enriched for the gene expression microarray analysis, which was performed using SurePrint G3 Human Gene Expression 8X60K microarrays.

Dataset Information

MicroRNA profiling of in vitro grass pollen extract (allergen) challenged CD4+T-cells against paired unchallenged controls from Seasonal Allergic Rhinitis patients

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