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Links from GEO DataSets

Items: 9

1.
Full record GDS4116

Diabetogenic BDC T-cell transfer model of type I diabetes: pancreatic islets

Analysis of pancreatic islets after injection of diabetogenic BDC CD4 T cells into nondiabetic NOD Rag1-/- recipients, 24 to 48 hrs post-transfer. Results provide insight into molecular mechanisms underlying the T-cell entry induced state of receptivity of islets to subsequent immunological insults.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 cell type, 2 genotype/variation, 3 protocol, 3 time sets
Platform:
GPL6246
Series:
GSE26147
13 Samples
Download data: CEL, CHP
2.

Examination of inflammatory transcripts during a transfer model of type I diabetes.

(Submitter supplied) In an accompanying paper we found specific localization of diabetogenic T cells only to islets of Langerhans bearing the specific antigen. Instrumental in the specific localization was the presence of intra-islet dendritic cells bearing the β-cell-peptide-MHC complex. Here we report that the entry of diabetogenic CD4 T cells very rapidly triggered inflammatory gene expression changes in islets and vessels by up-regulating chemokines and adhesion molecules. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Datasets:
GDS4115 GDS4116
Platform:
GPL6246
20 Samples
Download data: CEL, CHP
Series
Accession:
GSE26147
ID:
200026147
3.
Full record GDS4115

Diabetogenic 3A9 T-cell transfer model of type I diabetes: pancreatic islets

Analysis of islet cells after injection of diabetogenic 3A9 CD4 T cells into nondiabetic B10.BR IP-HEL recipients, 8 to 24 hrs post-transfer. Results provide insight into molecular mechanisms underlying the T-cell entry induced state of receptivity of islets to subsequent immunological insults.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 genotype/variation, 2 protocol, 3 time sets
Platform:
GPL6246
Series:
GSE26147
7 Samples
Download data: CEL, CHP
4.

Interferon-γ-dependent regulatory circuits in immune inflammation highlighted in diabetes

(Submitter supplied) We demonstrate diverse roles of interferon–gamma (IFN-γ) in the induction and regulation of immune-mediated inflammation using a transfer model of autoimmune diabetes. The diabetogenic CD4+BDC2.5 (BDC) T cell clone upon transfer into NOD.scid mice induced destruction of islets of Langerhans leading to diabetes. Administration of a neutralizing antibody to IFN-γ (H22) resulted in long term protection (LTP) from diabetes, with inflammation but persistence of a significant, albeit decreased numbers of β-cells. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS4034
Platform:
GPL1261
8 Samples
Download data: CEL
Series
Accession:
GSE12389
ID:
200012389
5.
Full record GDS4034

Time course of diabetes-induced, anti-Interferon-γ injected NOD.Scid mice: pancreatic islets

Temporal analysis of microdissected islets of NOD.Scid mice injected with diabetogenic CD4+BDC2.5 (BDC) T cells, then injected with anti-interferon-γ monoclonal antibody which protected the mice from developing diabetes. Results provide insight into the role of INF-γ role in autoimmune diabetes.
Organism:
Mus musculus
Type:
Expression profiling by array, transformed count, 2 agent, 2 protocol, 5 time sets
Platform:
GPL1261
Series:
GSE12389
8 Samples
Download data: CEL
6.

Genome-wide transcriptional analyses of islet-specific CD4+ T cells identify Idd9 genes controlling diabetogenic T cell function

(Submitter supplied) Analysis of gene expression levels in ex-vivo and p79-stimulated splenic CD4+ T cells.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL14828
12 Samples
Download data: TXT
Series
Accession:
GSE64674
ID:
200064674
7.

Progression to Islet Destruction in a Cyclophosphamide-Induced Transgenic Model

(Submitter supplied) BDC2.5/NOD mice were treated with cyclophosphamide to induce type 1 diabetes. Their pancreatic islets were analyzed before treatment (Day 0) and as treatment progressed (Days 1 through 3) Keywords = type I diabetes Keywords = cyclophosphamide Keywords = BDC2.5 Keywords = NOD Keywords = pancreas Keywords = islets Keywords: time-course
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS1056
Platform:
GPL81
18 Samples
Download data
Series
Accession:
GSE2254
ID:
200002254
8.
Full record GDS1056

Type 1 diabetes model response to cyclophosphamide: time course

Analysis of pancreatic islets from BDC2.5/NOD transgenics after treatment with 200 mg/kg cyclophosphamide (CY) at various time points up to 3 days. CY induces diabetes in BDC2.5/NOD transgenics. Results provide insight into molecular events accompanying the progression from insulitis to diabetes.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 agent, 4 time sets
Platform:
GPL81
Series:
GSE2254
18 Samples
Download data
DataSet
Accession:
GDS1056
ID:
1056
9.

Transcriptional analysis of type 1 diabetes reveals an interferon signature that precedes T cell activation

(Submitter supplied) Type 1 diabetes (T1D) is an autoimmune disease triggered by T cell reactivity to protein antigens produced by the β-cells. Here we present a chronological compendium of transcriptional profiles from islets of Langerhans isolated from non-obese diabetic (NOD) mice ranging from 2 wks up to diabetes and compared to controls. Parallel analysis was made of cellular components of the islets. Myeloid cells populated the islets early during development in all mouse strains. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
57 Samples
Download data: CEL
Series
Accession:
GSE41203
ID:
200041203
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