Mus musculus strain:NOD/ShiLtJ
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ABSTRACT:
PROVIDER: PRJNA205205 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Profiles of gene expression in salivary gland cells were compared between NOD/ShiLtJ mice, an animal model or Sjogren's syndrome with or without T1D. We used microarrays to detail the global programme of gene expression when type 1 diabetes and identified distinct classes of up- or down-regulated genes.
2021-07-09 | GSE179654 | GEO
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
Project description:Protein source in diet greatly influences the incidence of type-1 diabetes (T1D) in non-obese diabetic (NOD) mouse colonies. NOD mice fed a diet containing hydrolyzed casein (HC) as the sole protein source are protected from T1D. Replacing 1/5th of the HC with gluten restores high T1D to NOD mice. We hypothesized that gluten might promote inflammation in the islets. We used single cell RNA sequencing (scRNAseq) to characterize and contrast the transcriptional profiles of endocrine cells and islet infiltrating leukocytes from the pancreatic islets of Langerhans of NOD mice fed a 20% HC diet or a 16% HC + 4% gluten diet.
2023-01-04 | GSE217493 | GEO
Project description:Expression data from salivary gland cells of NOD/shiLtJ mice and NOD/shiLtJ mice with type 1 diabetes
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Project description: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.
2021-11-16 | GSE183286 | GEO
Project description:Hybrid insulin peptides (HIPs) form in pancreatic beta cells through the covalent cross-linking of proinsulin peptides with various beta cell peptides, creating unique amino acid sequences not encoded in the genome. HIPs have been confidently identified in both human and mouse islets by mass spectrometry and are targeted by autoreactive T cells in type 1 diabetes (T1D) patients and disease-triggering CD4 T cells in non-obese diabetic (NOD) mice. Previous work identified cathepsin D (CatD) as an enzyme involved in HIP formation through transpeptidation reactions targeting a conserved leucine residue (L26) in the C-peptide region of proinsulin. In this study, we generated NOD mice with a leucine-to-isoleucine substitution at this position in the insulin 2 gene (NOD INS2I/I) to prevent CatD-mediated HIP formation. Mass spectrometry analysis of islet peptidomes revealed that the L26I modification effectively blocked CatD-mediated cleavage at this site and significantly reduced the levels of disease-relevant HIPs, including HIP11 and 6.9HIP. These findings were validated through T cell assays showing reduced antigenicity of islets from modified mice when exposed to HIP-reactive T cell clones. The functional consequences of reduced HIP formation were demonstrated in a year-long monitoring study, where NOD INS2I/I mice exhibited significantly delayed disease onset compared to wild-type NOD mice, with 43% versus 10% remaining disease-free after one year. In vitro experiments with human C-peptide further confirmed that the L26I substitution prevents CatD-mediated HIP formation in human samples as well. Our results establish CatD as the primary enzymatic driver of disease-relevant HIP formation and demonstrate that preventing CatD-mediated processing of proinsulin 2 C-peptide in NOD mice significantly reduces HIP formation and delays autoimmune diabetes progression, identifying a potential therapeutic target for T1D prevention.
2025-12-22 | PXD063329 | Pride
Project description:Single cell RNA sequencing on pancreatic islet infiltrating T cells from NOD mice.
| PRJNA1037506 | ENA
Project description:With the goal of identifying changes in gene expression in CD4(+) T cells during the development of diabetes in the nonobese diabetic (NOD) mouse, we used DNA microarrays to analyze gene expression in CD4(+) T cells from the pancreatic draining lymph nodes of NOD/BDC 2.5 T cell receptor transgenic and WT NOD mice at different ages. At 4 and 6 weeks of age, we found up-regulation of a number of genes that are known to be induced by IFN-alpha. IFN-alpha levels and IFN-alpha-producing plasmacytoid dendritic cells were increased in the PLNs of 3- to 4-week-old NOD mice. Moreover, blockade of IFN-alpha receptor 1 in NOD mice by a neutralizing antibody at 2-3 weeks of age significantly delayed the onset and decreased the incidence of type 1 diabetes, increased the relative number of immature dendritic cells in the PLNs, and enhanced the ability of spleen CD4(+) T cells to produce IL-4 and IL-10. These findings demonstrate that IFN-alpha in the PLNs is an essential initiator in the pathogenesis of type 1 diabetes in NOD mice.
2009-03-13 | GSE15213 | GEO
Project description:T cells infiltrate pancreatic islets during the progression of type 1 diabetes (T1D) but their differentiation states have not been completely defined. We used unbiased single-cell RNA sequencing analyses to gain further insight into the phenotypic complexity of islet-infiltrating T cells in non-obese diabetic (NOD) mice. In the CD4 T cell compartment, we identified naïve, memory, and regulatory T cells, as well as multiple Il21 expressing effector subsets positive for markers indicative of Th1 and Tfh cells. In CD8 T cells, we identified two activated subsets in addition to naïve cells. The two activated islet CD8 T cell subsets respectively resemble the self-renewing progenitor cells and the terminally differentiated/exhausted effectors during chronic lymphocytic choriomeningitis virus infection. We also identified a BATF-driven transcriptional signature promoting the diabetogenic activity of islet-infiltrating β cell autoreactive CD8 T effectors. Our results provide a useful resource for understanding T cell differentiation programs in T1D.
2024-01-22 | GSE125454 | GEO
Project description:T cells infiltrate pancreatic islets during the progression of type 1 diabetes (T1D) but their differentiation states have not been completely defined. We used unbiased single-cell RNA sequencing analyses to gain further insight into the phenotypic complexity of islet-infiltrating T cells in non-obese diabetic (NOD) mice. In the CD4 T cell compartment, we identified naïve, memory, and regulatory T cells, as well as multiple Il21 expressing effector subsets positive for markers indicative of Th1 and Tfh cells. In CD8 T cells, we identified two activated subsets in addition to naïve cells. The two activated islet CD8 T cell subsets respectively resemble the self-renewing progenitor cells and the terminally differentiated/exhausted effectors during chronic lymphocytic choriomeningitis virus infection. We also identified a BATF-driven transcriptional signature promoting the diabetogenic activity of islet-infiltrating β cell autoreactive CD8 T effectors. Our results provide a useful resource for understanding T cell differentiation programs in T1D.
2024-01-22 | GSE125452 | GEO