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Single-cell RNA sequencing of murine islets shows high cellular complexity at all stages of autoimmune diabetes

ABSTRACT: Single-cell RNA sequencing of murine islets shows high cellular complexity at all stages of autoimmune diabetes

PROVIDER: PRJNA594724 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10662100.fastq.gz	Fastqsanger.gz
	SRR10662101.fastq.gz	Fastqsanger.gz
	SRR10662102.fastq.gz	Fastqsanger.gz
	SRR10662103.fastq.gz	Fastqsanger.gz
	SRR10662104.fastq.gz	Fastqsanger.gz

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Single-cell RNA sequencing of murine islets shows high cellular complexity at all stages of autoimmune diabetes

Project description:Single-cell RNA sequencing of murine islets shows high cellular complexity at all stages of autoimmune diabetes

| PRJNA594719 | ENA

Single-cell RNA sequencing of murine islets shows high cellular complexity at all stages of autoimmune diabetes

Project description:Tissue-specific autoimmune diseases are driven by activation of diverse immune cells in the target organs. However, the molecular signatures of immune cell populations over time in an autoimmune process remain poorly defined. Using single-cell RNA sequencing, we performed an unbiased examination of diverse islet-infiltrating cells during autoimmune diabetes in the nonobese diabetic mouse. The data revealed a landscape of transcriptional heterogeneity across the lymphoid and myeloid compartments. Memory CD4 and cytotoxic CD8 T cells appeared early in islets, accompanied by regulatory cells with distinct phenotypes. Surprisingly, we observed a dramatic remodeling in the islet microenvironment, in which the resident macrophages underwent a stepwise activation program. This process resulted in polarization of the macrophage subpopulations into a terminal proinflammatory state. This study provides a single-cell atlas defining the staging of autoimmune diabetes and reveals that diabetic autoimmunity is driven by transcriptionally distinct cell populations specialized in divergent biological functions.

2020-03-27 | GSE141786 | GEO

Single-cell RNA sequencing of murine islets shows high cellular complexity at all stages of autoimmune diabetes

Project description:Tissue-specific autoimmune diseases are driven by activation of diverse immune cells in the target organs. However, the molecular signatures of the immune cell populations over time in an autoimmune process remain poorly defined. Using single-cell RNA sequencing, we performed unbiased examination of diverse islet-infiltrating cells during autoimmune diabetes in the non-obese diabetic mouse. The data revealed a landscape of transcriptional heterogeneity across the lymphoid and myeloid compartments. Memory CD4 and cytotoxic CD8 T cells appeared early in islets accompanied by regulatory cells with distinct phenotypes. Surprisingly, we observed a dramatic remodeling in the islet microenvironment, in which the resident macrophages underwent a stepwise activation program. This process resulted in polarization of the macrophage subpopulations into a terminal pro-inflammatory state. This study provides a single-cell atlas defining the staging of autoimmune diabetes and reveals that diabetic autoimmunity is driven by transcriptionally distinct cell populations specialized in divergent biological functions.

2020-03-27 | GSE141784 | GEO

Single-cell RNA sequencing of murine islets shows high cellular complexity at all stages of autoimmune diabetes.

| S-EPMC7971127 | biostudies-literature

Inflammatory profile of NOD.Batf3-/- islets

2014-09-29 | GSE61847 | GEO

Inflammatory profile of NOD.Batf3-/- islets

Project description:NOD mice deficient in the transcription factor Batf3 never develop diabetes. The goal of this study was to determine if NOD.Batf3-/- mice islets had any inflammatory signature associated with type 1 diabetes. Islets of Langerhans were isolated from NOD, NOD.Batf3-/-, and NOD.Rag1-/- and then compared to determine inflammatory gene profiles. At 6 and 8 weeks of age, NOD.Batf3-/- islets had an absence of inflammatory gene expression and were almost identical to uninflamed NOD.Rag1-/- islets. This work shows that absence of the Batf3 transcription factor is sufficient to prevent all the inflammatory sequelae of autoimmune diabetes. RNA was isolated from the pancreatic islets of Langerhans of 27 experimental mice. Mice were aged either 6 or 8 weeks. Three genotypes were tested: NOD, NOD.Rag1-/-, and NOD.Batf3-/-. There were 3-6 biological replicates per condition. All mice were female. All data was normalized using RMA in Arraystar.

2014-09-29 | E-GEOD-61847 | biostudies-arrayexpress

Inhibition of the Eukaryotic Initiation Factor-2-α Kinase PERK Decreases Risk of Autoimmune Diabetes in Mice

Project description:Prevention or delay of autoimmune type 1 diabetes (T1D) onset is possible if molecular triggering events can be pharmacologically targeted. The integrated stress response (ISR) is activated during cellular stress to halt protein production and redirect energy towards cellular survival temporarily. We hypothesized that the activity of the ISR in the insulin-producing β cell during T1D becomes maladaptive and renders the cell prone to autoimmunity. We show that suppression of the ISR by using a novel inhibitor of the kinase PERK reverses the translation initiation block in stressed human islets and delays the onset of diabetes, reduces islet inflammation, and preserves β cell mass in T1D-susceptible mice. Single-cell RNA sequencing of islets from PERK-inhibited mice shows reductions in the unfolded protein response and PERK signaling pathways and alterations in antigen processing and presentation pathways in β cells. Spatial proteomics analysis of islets from these mice shows a post-transcriptional increase in the immune checkpoint protein PD-L1 in β cells. Golgi membrane protein 1, whose levels increase following ISR inhibition in human islets and EndoC-βH1 human β cells, interacts with and post-transcriptionally stabilizes PD-L1. Collectively, our studies show that the ISR, mediated by PERK, enhances β cell immunogenicity, and inhibition of PERK may offer a strategy to prevent or delay the development of T1D.

2024-06-05 | GSE245004 | GEO

Crinophagic granules in pancreatic β cells contribute to mouse autoimmune diabetes by diversifying pathogenic epitope repertoire

Project description:We examined the transcriotional changes in antigen specific CD4 T cells to antigens derived from thymus or to the antigens derived from islets in the autoimmune diabetes mouse model.

2024-09-06 | GSE275211 | GEO

A dormant T cell population with autoimmune potential exhibits low self-reactivity and infiltrates islets in type I diabetes

Project description:T cells have been established as the key drivers of autoimmune diabetes. However, it is unknown whether all T cells that infiltrate the pancreas are equally pathogenic, and how the level of reactivity for self-antigen modulates differentiation and pathogenic potential of effector T cells. Moreover, the contribution of bystander, non-antigen reactive T cells in islet autoimmunity has not been resolved. Using multi-color flow cytometry in combination with Nur77-GFP reporter of TCR signaling we identified a “dormant” population of CD4+ T cells that infiltrate the islets of pre-diabetic NOD mice and constitute a significant proportion of all islet infiltrating T cells (~47%). We analyzed TCR repertoire, transcriptional profile, effector function, and autoimmune potential of this subpopulation. This T cell population, characterized by low level expression of CD5 and a unique TCR repertoire, exhibited central memory phenotype with reduced activation and effector function; however, induced rapid diabetes upon transfer. Overall, our study suggests that the strength of reactivity for tissue antigen dictates the level of T cell activation and differentiation; however, cells with low level of TCR signaling and reactivity for islet antigen infiltrating the pancreas of NOD mice are pathogenic and are capable of inducing beta cell destruction.

2019-05-17 | GSE131345 | GEO

Treg insufficiency in autoimmune diabetes is driven by selective loss of Neuropilin-1 on intra-islet regulatory T cells

Project description:Strategies targeting Treg insufficiency are vital for treating autoimmune diseases like T1D. Our findings highlight the critical role of Neuropilin 1 (Nrp1) in stabilizing Tregs within pancreatic islets. Boosting Nrp1 levels delays diabetes onset by enhancing Treg function. This underscores Nrp1 as a potential target for bolstering Treg activity and combating autoimmune diseases.

2024-08-10 | GSE262874 | GEO

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