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Comparative assessment of the transcriptome of pancreatic islets from Non-Obese Diabetic mice in the absence of immune infiltrate

ABSTRACT: The transcriptome of pancreatic islets from four mouse strains was compared - NODk.RagKO, B10k.RagKO, NODk.RagKO.insHEL and B10k.RagKO.insHEL. This comparison allows the assessment of altered transcriptome due to two factors - genetic background of NOD vs B10 strain, and the effect of the insHEL transgene. The use of the MHC k haplotype and the RagKO background remove contamination from infiltrating immune cells, in order to obtain a pure islet transcriptome.

ORGANISM(S): Mus musculus

PROVIDER: GSE56507 | GEO | 2016/02/23

SECONDARY ACCESSION(S): PRJNA243560

REPOSITORIES: GEO

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Comparative assessment of the transcriptome of pancreatic islets from Non-Obese Diabetic mice in the absence of immune infiltrate

Project description:The transcriptome of pancreatic islets from four mouse strains was compared - NODk.RagKO, B10k.RagKO, NODk.RagKO.insHEL and B10k.RagKO.insHEL. This comparison allows the assessment of altered transcriptome due to two factors - genetic background of NOD vs B10 strain, and the effect of the insHEL transgene. The use of the MHC k haplotype and the RagKO background remove contamination from infiltrating immune cells, in order to obtain a pure islet transcriptome. Three mice of each gentoype were analyzed in this study.

2016-02-23 | E-GEOD-56507 | biostudies-arrayexpress

Comparison of gene expression between islets from NOD-Rag and NOD-Idd22 mice

Project description: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.

2022-06-27 | GSE206705 | GEO

Coxsackievirus B3 (CVB3) infection of AJ, B10.A, CSS3 and B6.chr3AJ (heart tissue day 4)

Project description:The pathogenesis of viral myocarditis is a multifactorial process involving host genetics, viral genetics and the environment in which they interact. Here, we used a model of infection with Coxsackievirus B3 to characterize the contribution of host genetics to viral myocarditis. We determined heart CVB3 load in mice from a classical intercross between progenitors A/J (H2a) and B10.A-H2a (B10.A) of different genetic backgrounds but with a common H2 haplotype. Here we compare whole genome expression patterns in infected and uninfected A/J and B10.A mice in order to determine which gene expression programs are common or distinct to each strain.

2011-05-01 | GSE19496 | GEO

Coxsackievirus B3 (CVB3) infection of AJ, B10.A, CSS3 and B6.chr3AJ (heart tissue day 4)

2011-05-01 | E-GEOD-19496 | biostudies-arrayexpress

Comparison of gene expression profiles in NOD and Idd9 CD4+ T cells

Project description:Nonobese diabetic (NOD) mice congenic for B10 derived genes in the Idd9 region of chromosome 4 are highly protected from the development of diabetes. In order to identify possible candidate genes within the Idd9 susceptibility region and possible downstream mediators of protection, we compared gene expression between NOD and Idd9 CD4+ T-cells. CD4+ T-cells with an activated phenotype (CD44-high/CD62L-low) were sorted from the pancreatic lymph nodes of female 8-week old mice. Mice were bred at Taconic farms and were line 905 (NOD.B10-Idd9 congenic) and line 6359 (NOD-like control strain with a B10 congenic region on chromosome 1 which does not modify diabetes incidence). Three replicate samples were prepared, each from four pooled pancreatic lymph nodes. CD4+CD44-highCD62L-low T-cells were sorted from each sample.

2012-02-01 | E-GEOD-35482 | biostudies-arrayexpress

Effect of the Idd2 locus of B10 origin on the transcriptome of B cell of NOD mice

Project description:Type 1 diabetes (T1D) is an autoimmune disease characterized by pancreatic beta-cell destruction. It is a complex genetic trait driven by over 30 genetic loci with parallels between humans and mice. The NOD mouse spontaneously develops autoimmune diabetes and is widely used to identify insulin-dependent diabetes (Idd) genetic loci linked to diabetes susceptibility. While many Idd loci have been extensively studied, the impact of the Idd2 locus on autoimmune diabetes susceptibility remains to be defined. To address this, we generated a NOD congenic mouse bearing B10 resistance alleles on chromosome 9 in a locus coinciding with part of the Idd2 locus and find that NOD.B10-Idd2 congenic mice are highly resistant to diabetes. Bone marrow chimera and adoptive transfer experiments show that the B10 protective alleles provide resistance in an immune cell-intrinsic manner. While no T cell-intrinsic differences between NOD and NOD.B10-Idd2 mice were observed, we find that the Idd2 resistance alleles limit the formation of spontaneous and induced germinal centers. Comparison of the B cell transcriptome profile from NOD and NOD.B10-Idd2 mice reveal that resistance alleles at the Idd2 locus affect the expression of specific MHC molecules, a result confirmed by flow cytometry. Altogether, these data demonstrate that resistance alleles at the Idd2 locus impair germinal center formation and influence MHC expression, both of which likely contribute to reduce diabetes incidence.

2022-10-06 | GSE185487 | GEO

Gene expression in the islets of 12 wk old Non-Obese Diabetic (NOD) mice and healthy control NOD.B10 mice

Project description:Gene expression in the islets of NOD and NOD.B10 mice at 12 weeks of age, prior to the onset of destructive insulitis.

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Analysis of a non-obese diabetes-experimental autoimmune encephalomyelitis (NOD-EAE)

Project description:The purpose of this study was to analyze and elucidate the mechanisms of non-obese diabetes-experimental autoimmune encephalomyelitis (NOD-EAE), an animal model of progressive multiple sclerosis (MS), and to compare the pathological features with those observed in human progressive MS. To achieve this, pathological analysis, flow cytometry analysis, immunohistochemical staining, and transcriptome analysis were performed at each pathological stage of the NOD-EAE mice to characterize each pathological stages in the lesion. In the chronic phase of the NOD-EAE mice, fibrosis and lymph follicle formation, characteristic of progressive human MS, were observed. We describe the pathological profile and transcriptome analysis of the NOD-EAE mice and verify that this model has similar features to those of human progressive MS. Our findings suggest that this model recapitulates lymph follicle formation, a disease hallmark of progressive MS, and fibrosis, a feature complicating the pathogenesis of MS in the chronic phase.

2024-04-01 | GSE243235 | GEO

Comparison of gene expression profiles in NOD and Idd9 CD4+ T cells

2012-02-01 | GSE35482 | GEO

Proteomic identification of MHC class I-associated peptidome derived from non-obese diabetic mouse thymus and pancreas

Project description:The peptides repertoire presented to CD8+ T cells by major histocompatibility complex (MHC) class I molecules, referred to as the MHC I-associated peptidome (MIP), regulates all critical events that occur during the lifetime of CD8+ T cells. The MIP presented by thymic antigen presenting cells (APCs) is crucial for shaping CD8+ T cell repertoire and self-tolerance, while the MIP presented by peripheral tissues and organs is not only involved in maintaining periphery CD8+ T cell survival and homeostasis, but also mediates immune surveillance and autoimmune responses of CD8+ T cells under pathological conditions. Type 1 diabetes (T1D) is an organ-specific autoimmune disease caused by the destruction pancreatic β cells, mediated primarily by autoreactive CD8+ T cells. Non-obese diabetic (NOD) mouse is one of important animal models of spontaneous autoimmune diabetes that shares several key features with human T1D. Here, we deeply analyzed the MIP derived from the primary tissues of thymus and pancreas in NOD mice using targeted database searches of mass spectrometry data. We demonstrated that the thymus MIP source proteins accommodated only a small portion of the transcriptome of thymus epithelial cells, and partially shared with the MIP source proteins derived from NOD mice pancreas and β cell line. The global view of the MHC I-associated self-peptides repertoire in the thymus and pancreas of NOD mice may serve as a biological reference to identify potential autoantigens targeted by autoreactive CD8+ T cells in T1D.

2022-10-14 | PXD031966 | Pride

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