GEO DataSets

Analysis of anti-IgM-F(ab’)2 fragment-stimulated, splenic B cells from non-obese diabetic (NOD) or NR4 (NOD background with Chromosome 4, type 1 diabetes (T1D)-resistance alleles) females. Results provide insight into the molecular mechanisms underlying NOD and NR4 diabetogenic activity.

Organism:

Mus musculus

Type:

Expression profiling by array, transformed count, 2 agent, 2 strain sets

Platform:

GPL1261

Series:

GSE37294

11 Samples

Download data: CEL

(Submitter supplied) Type 1 Diabetes (T1D) in humans and the non-obese diabetic (NOD) mouse model results from autoreactive T cell destruction of pancreatic beta cells. A pathogenic role for B lymphocytes (B cells) in T1D first became evident when NOD mice made deficient in this population through introduction of an inactivated Igµ heavy chain gene (NOD.Igµnull) or chronic treatment with anti-IgM antibodies were strongly protected from disease. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS4340

Platform:

GPL1261

11 Samples

Download data: CEL

(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

(Submitter supplied) To characterize B6.H2g7 Vb3+(Trbv26+) CD4+ T-cells, which are deleted by NOD-encoded Mtv3 in B6.H2g7.Idd32NOD/NOD mice, paired single-cell RNA sequencing and single-cell TCR sequencing was performed on two separate pools of B6.H2g7 CD4+ T-cells 14 days after they were adoptively transferred into two NOD.Rag1null recipient mice.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

4 Samples

Download data: CSV, MTX, TSV

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by RT-PCR; Expression profiling by high throughput sequencing

Platforms:

GPL26927 GPL16417

1845 Samples

Download data: XLS, XLSX

(Submitter supplied) Abstract- The class II region of the Major Histocompatibility locus is the main contributor to the genetic susceptibility to type 1 diabetes (T1D). The loss of an aspartic acid at position 57 of diabetogenic HLA-DQ8 chains supports this association; it influences the recognition of peptides in the context of HLA-DQ8, and I-Ag7 using a mechanism termed the P9 switch. Here, we built register-specific insulin MHC tetramers, Ins12-20 and Ins13-21, to examine anti-insulin CD4 T cell responses during the early pre-diabetic phase of disease in mice. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16417

16 Samples

Download data: XLS, XLSX

(Submitter supplied) Abstract- The class II region of the Major Histocompatibility locus is the main contributor to the genetic susceptibility to type 1 diabetes (T1D). The loss of an aspartic acid at position 57 of diabetogenic HLA-DQ8 chains supports this association; it influences the recognition of peptides in the context of HLA-DQ8, and I-Ag7 using a mechanism termed the P9 switch. Here, we built register-specific insulin MHC tetramers, Ins12-20 and Ins13-21, to examine anti-insulin CD4 T cell responses during the early pre-diabetic phase of disease in mice. more...

Organism:

Mus musculus

Type:

Expression profiling by RT-PCR

Platform:

GPL26927

1829 Samples

Download data: CSV

(Submitter supplied) To gain further insight into potential specific gene signatures expressed by pancreatic islet cells and pathogenic CD4+ T lymphocytes isolated from sublines of non-obese diabetic (NOD) mice expressing high or low autoimmune (type 1) diabetes incidence.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL10787

50 Samples

Download data: TXT

(Submitter supplied) Type 1 diabetes is a multigenic disease caused by T-cell mediated destruction of the insulin producing β-cells. Although conventional (targeted) approaches of identifying causative genes have advanced our knowledge of this disease, many questions remain unanswered. Using a whole molecular systems study, we unraveled the genes/molecular pathways that are altered in CD4 T-cells from young NOD mice prior to insulitis (lymphocytic infiltration into the pancreas). more...

Organism:

Mus musculus

Type:

Expression profiling by array

Datasets:

GDS5018 GDS5019 GDS5020

Platform:

GPL1261

44 Samples

Download data: CEL

Analysis of CD4 T-cells from 4-week old NOD females in the preinsulitis stage of Type 1 diabetes. Control strains NOR (~88% similarity to NOD genome) and C57BL/6 (genetically distant) are both insulitis- and diabetes-free. Results provide insight into molecular basis of CD4 T-cell diabetogenesis.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 disease state, 3 strain sets

Platform:

GPL1261

Series:

GSE46600

15 Samples

Download data: CEL

Analysis of CD4 T-cells from 3-week old NOD females in the preinsulitis stage of Type 1 diabetes. Control strains NOR (~88% similarity to NOD genome) and C57BL/6 (genetically distant) are both insulitis- and diabetes-free. Results provide insight into molecular basis of CD4 T-cell diabetogenesis.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 disease state, 3 strain sets

Platform:

GPL1261

Series:

GSE46600

15 Samples

Download data: CEL

Analysis of CD4 T-cells from 2-week old NOD females in the preinsulitis stage of Type 1 diabetes. Control strains NOR (~88% similarity to NOD genome) and C57BL/6 (genetically distant) are both insulitis- and diabetes-free. Results provide insight into molecular basis of CD4 T-cell diabetogenesis.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 disease state, 3 strain sets

Platform:

GPL1261

Series:

GSE46600

14 Samples

Download data: CEL

(Submitter supplied) Both immunodeficient and wild type NOD mice exhibit defects in control of early T-cell development in the thymus. We show that Rag1-deficient NOD mice fail to enforce both the b-selection checkpoint and an earlier T-cell commitment checkpoint, based on genome-wide genetic and transcriptome analyses. A major QTL peak for the checkpoint breakthrough phenotype mapped to the diabetes susceptibility Idd9/11 region, as confirmed by congenic mouse analysis. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL9250

4 Samples

Download data: RPKM

(Submitter supplied) NOD-Idd22 mice are congenic mice of NOD background with a piece of chromosome 8 being substituted with ALR genetic material. These mice are resistant to spontaneous autoimmune diabetes as well as chemically induced in vivo islet beta cell destructions. The goal of this project is to come pare gene expressions in islets between NOD-Idd22 and NOD mice. NOD-Rag1 was used instead of NOD to avoid lymphocyte infiltrtation in isltes.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL16570

7 Samples

Download data: CEL, TXT