Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling human whole blood from children with pre-type1diabetes


ABSTRACT: Type 1 diabetes (T1D) is an autoimmune disease caused by selective destruction of insulin producing pancreatic beta-cells in the islets of the Langerhans. The progression to clinical diabetes is characterized by the appearance of autoantibodies against islet cells (ICA) and beta-cell-specific antigens (IAA, IA-2 and GADA), which are considered the first markers signifying onset of autoimmunity. The mechanisms initiating or enhancing the autoimmune process remain poorly understood. Transcriptomic profiling on whole blood samples provides an approach for monitoring T1D disease process. In these investigations of pathways that are changed during the disease process, we have analyzed RNA from longitudinal peripheral blood samples of children who have developed T1D associated autoantibodies and eventually clinical type 1 diabetes . All study subjects were participants of the Type 1 Diabetes Prediction and Prevention (DIPP) study in Finland (38). Whole-blood RNA samples were collected during periodic clinic visits, typically at 3 to 12 month intervals. 2.5 ml venous blood was drawn into PAXgene Blood RNA tubes (Becton-Dickinson) and stored at -70°C. T1D-associated autoantibodies were measured from blood samples taken at each visit. Prospective samples from 3 children who developed T1D (subjects T1D_1 - T1D_3) and 2 children who developed ICA (subjects ICA_1 and ICA_2) during the DIPP follow-up were selected to the present study. Control children for the T1D cases (subjects T1D_C1 - T1D_C2) were matched for age, gender, birth place and HLA-genotype, from families who have no first-degree relatives with T1D. All samples (n=60) were processed and hybridized on Affymetrix Human Genome U133 Plus 2.0 arrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Juha Mykkänen 

PROVIDER: E-TABM-666 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Early suppression of immune response pathways characterizes children with prediabetes in genome-wide gene expression profiling.

Elo Laura L LL   Mykkänen Juha J   Nikula Tuomas T   Järvenpää Henna H   Simell Satu S   Aittokallio Tero T   Hyöty Heikki H   Ilonen Jorma J   Veijola Riitta R   Simell Tuula T   Knip Mikael M   Simell Olli O   Lahesmaa Riitta R  

Journal of autoimmunity 20100330 1


Type 1 diabetes (T1D) is caused by autoimmune destruction of insulin-producing pancreatic beta cells in the islets of Langerhans. Although defects in various T cell subsets have been linked to the disease pathogenesis, mechanisms initiating or enhancing the autoimmunity in prediabetes remain poorly understood. To unravel genes and molecular pathways affected by the diabetes-associated autoimmunity, we investigated transcriptomic profiles of prospective whole-blood samples from children who have  ...[more]

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