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Repertoire analysis of the repertoire of insulin-reactive B cells in type 1 diabetes-prone mice

ABSTRACT: Repertoire analysis of the repertoire of insulin-reactive B cells in type 1 diabetes-prone mice

PROVIDER: PRJNA883394 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21678183_1.fastq.gz	Fastqsanger.gz
	SRR21678183_2.fastq.gz	Fastqsanger.gz
	SRR21678184_1.fastq.gz	Fastqsanger.gz
	SRR21678184_2.fastq.gz	Fastqsanger.gz
	SRR21678185_1.fastq.gz	Fastqsanger.gz

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Repertoire analysis of the repertoire of insulin-reactive B cells in type 1 diabetes-prone mice

Project description:Seropositivity for autoantibodies against islet autoantigens is associated with the development of autoimmune type 1 diabetes and B cell targeted therapies are effective in both mouse models and in patients who are affected by or at risk for autoimmune type 1 diabetes. The role of B cell receptor affinity in autoimmune type 1 diabetes is unclear. Here, we employed single cell RNA sequencing to define the relationship between B cell receptor affinity for insulin and B cell phenotype during disease development using immunoglobulin heavy chain (VH125) transgenic mouse model (VH125.NOD) in which insulin binding B cells lose self-tolerance, becoming activated during development of autoimmmun type 1 diabetes.

2022-09-26 | GSE213973 | GEO

Protective role of gut insulin action in the development of nonalcoholic steatohepatitis and hepatocellular carcinoma associated with diabetes in mice

Project description:Diabetes is known to increase the risk of nonalcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC). Here we treated STAM (STelic Animal Model) mice, which develop diabetes, NASH and HCC associated with dysbiosis upon low-dose streptozotocin and high-fat diet (HFD), with insulin or phlorizin. Although both treatments ameliorated hyperglycemia and NASH, insulin treatment alone led to suppression of HCC accompanied by improvement of dysbiosis through restoration of antimicrobial peptide production. Similar changes in microflora are observed in insulin-treated patients comorbid with diabetes and NASH. Insulin treatment, however, failed to suppress HCC in the STAM mice lacking insulin receptor specifically in intestinal epithelial cells (ieIRKO), which showed dysbiosis and impaired gut barrier function. Furthermore, ieIRKO mice were prone to develop HCC merely on HFD. These data suggest that impaired gut insulin signaling increases the risk of HCC which can be countered by restoration of insulin action in diabetes.

2023-07-20 | GSE210876 | GEO

Protective role of gut insulin action in the development of nonalcoholic steatohepatitis and hepatocellular carcinoma associated with diabetes in mice

2023-07-20 | GSE210517 | GEO

Comparative analysis of the repertoire of insulin-reactive B cells in type 1 diabetes-prone and resistant mice.

Project description:Seropositivity for autoantibodies against multiple islet antigens is associated with development of autoimmune type 1 diabetes (T1D), suggesting a role for B cells in disease. The importance of B cells in T1D is indicated by the effectiveness of B cell-therapies in mouse models and patients. B cells contribute to T1D by presenting islet antigens, including insulin, to diabetogenic T cells that kill pancreatic beta cells. The role of B cell receptor (BCR) affinity in T1D development is unclear. Here, we employed single cell RNA sequencing to define the relationship between BCR affinity for insulin and B cell phenotype during disease development. We utilized immunoglobulin (Ig) heavy chain (VH125) mouse models in which high-affinity insulin-reactive B cells (IBCs) were previously shown to be anergic in diabetes-resistant VH125.C57BL/6-H2g7 and activated in VH125. NOD mice developing disease. Here, high-affinity IBCs were found in the spleen of prediabetic VH125. NOD mice and exhibited marginal zone or follicular phenotypes. Ig light chains expressed by these B cells are unmutated and biased toward Vκ4-74 and Vκ4-57 usage. Receptors expressed by anergic high-affinity IBCs of diabetes-resistant VH125.C57BL/6-H2g7 are also unmutated; however, in this genetic background light chains are polymorphic relative to those of NOD. Light chains derived from NOD and C57BL/6-H2g7 genetic backgrounds conferred divergent kinetics of binding to insulin when paired with the VH125 heavy chain. These findings suggest that relaxation of tolerance mechanisms in the NOD mouse leads to accumulation and partial activation of B cells expressing germline encoded high-affinity BCRs that support development of autoimmunity.

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Type 2 diabetes and insulin resistance

Project description:Global transcript profiling to identify differentially expressed skeletal muscle genes in insulin resistance, a major risk factor for Type II (non-insulin-dependent) diabetes mellitus. Compared gene expression profiles of skeletal muscle tissues from 18 insulin-sensitive versus 17 insulin-resistant equally obese, non-diabetic Pima Indians. Keywords: other

2002-12-17 | GSE121 | GEO

The repertoire of newly developing regulatory T cells in the type I diabetes-prone NOD mouse is very diverse

Project description:The repertoire of newly developing regulatory T cells in the type I diabetes-prone NOD mouse is very diverse

| PRJNA667334 | ENA

CD4+ T cells reactive to a hybrid peptide from insulin-chromogranin A adopt a distinct effector fate and are pathogenic in autoimmune diabetes

Project description:T cell-mediated islet destruction is a hallmark of autoimmune diabetes. Here, we examined the dynamics and pathogenicity of CD4+ T cell responses to four different insulin-derived epitopes during diabetes initiation in non-obese diabetic (NOD) mice. Single-cell RNA sequencing of tetramer-sorted CD4+ T cells from the pancreas revealed that islet-antigen-specific T cells adopted a wide variety of fates and required XCR1+ dendritic cells for their activation. Hybrid-insulin C-chromogranin A (InsC-ChgA)-specific CD4+ T cells skewed toward a distinct Th1 (T helper type 1) effector phenotype, whereas the majority of insulin B chain and hybrid-insulin C-islet amyloid polypeptide-specific CD4+ T exhibited a regulatory T cell phenotype and early or weak Th1 phenotype, respectively. InsC-ChgA-specific CD4+ T cells were uniquely pathogenic upon transfer, and an anti-InsC-ChgA:IAg7 antibody prevented spontaneous diabetes. Our findings highlight the heterogeneity of T cell responses to insulin-derived epitopes in diabetes and argue for the feasibility of antigen-specific therapies that blunts the response of pathogenic CD4+ T cells causing autoimmunity.

2025-06-17 | GSE275338 | GEO

The impact of aging on beta-cell functionality and structural integrity under metabolic stress conditions in diabetes-prone and diabetes-resistant mice.

Project description:Overnutrition contributes to insulin resistance, obesity and metabolic stress, initiating a loss of functional beta-cells and diabetes development. Whether these damaging effects are amplified in advanced age is barely investigated. Therefore, New Zealand Obese (NZO) mice, a well-established model for the investigation of human obesity-associated type 2 diabetes, were fed a metabolically challenging diet with a high-fat, carbohydrate restricted period followed by a carbohydrate intervention in young as well as advanced age. Interestingly, while young NZO mice developed massive hyperglycemia in response to carbohydrate feeding, leading to beta-cell dysfunction and cell death, aged counterparts compensated the increased insulin demand by persistent beta-cell function and beta-cell mass expansion. Beta-cell loss in young NZO islets was linked to increased expression of thioredoxin-interacting protein (TXNIP), presumably initiating an apoptosis-signaling cascade via caspase-3 activation. In contrast, islets of aged NZOs exhibited a sustained redox balance without changes in TXNIP expression, associated with higher proliferative potential by cell cycle activation. These findings support the relevance of a maintained proliferative potential and redox homeostasis for preserving islet functionality under metabolic stress, with the peculiarity that this adaptive response emerged with advanced age in diabetes-prone NZO mice.

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Metabolomic predictors of insulin resistance and diabetes

Project description:Metabolomic predictors of insulin resistance and diabetes

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Personalized Molecular Signatures of Insulin Resistance and Type 2 diabetes

Project description:Insulin resistance is a hallmark of type 2 diabetes, a highly heterogeneous condition with diverse pathological characteristics. Understanding the molecular adaptation to insulin resistance and its association with individual phenotypic traits is crucial for advancing precision medicine in diabetes. By utilizing cutting-edge proteomics technology, we mapped the proteome and phosphoproteome of basal and insulin-stimulated skeletal muscle from >120 individuals with varying degrees of insulin sensitivity, both with and without type 2 diabetes. Leveraging deep in vivo phenotyping data, we reveal that the basal proteome and phosphoproteome are strong predictors of insulin sensitivity. The insulin-stimulated phosphoproteome identified preserved and dysregulated signaling even in individuals with the most severe insulin resistance. Our study elucidates substantial differences in the male and female (phospho)proteome; however, the molecular signature associated with insulin resistance remains largely similar between sexes. These findings emphasize the importance of recognizing disease heterogeneity and advocate for the precision medicine approach for effective care in type 2 diabetes.

2025-05-27 | PXD049129 | Pride

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