Ontology highlight
ABSTRACT:
PROVIDER: PRJNA991778 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25193700.fastq.gz | Fastqsanger.gz | |||
| SRR25193701.fastq.gz | Fastqsanger.gz | |||
| SRR25193702.fastq.gz | Fastqsanger.gz | |||
| SRR25193703.fastq.gz | Fastqsanger.gz | |||
| SRR25193704.fastq.gz | Fastqsanger.gz |
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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. Exposure to HC also reduced beta-cell insulin secretion during glucose challenge suggesting that beneficial changes to beta-cell physiology might protect NOD mice from T1D. We used single cell RNA sequencing (scRNAseq) to contrast the transcriptional profiles of beta-cells and from the pancreatic islets of Langerhans of NOD mice with the scid mutation (scid mice were used to avoid confouding influence of infiltrating leukocytes) fed a 20% HC diet or a standard chow diet.
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Project description:Interventions: experimental group:fasting-mimicking diet;control group:none
Primary outcome(s): IgA+ B cells
Study Design: Parallel
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Project description:This a model from the article:
Modelling the onset of Type 1 diabetes: can impaired macrophage phagocytosis make the difference between health and disease?
Maree AF, Kublik R, Finegood DT, Edelstein-Keshet L.Philos Transact A Math Phys Eng Sci.2006 May 15;364(1842):1267-82.
16608707,
Abstract:
A wave of apoptosis (programmed cell death) occurs normally in pancreatic beta-cells of newborn mice. We previously showed that macrophages from non-obese diabetic (NOD) mice become activated more slowly and engulf apoptotic cells at a lower rate than macrophages from control (Balb/c) mice. It has been hypothesized that this low clearance could result in secondary necrosis, escalating inflammation and self-antigen presentation that later triggers autoimmune, Type 1 diabetes (T1D). We here investigate whether this hypothesis could offer a reasonable and parsimonious explanation for onset of T1D in NOD mice. We quantify variants of the Copenhagen model (Freiesleben De Blasio et al. 1999 Diabetes 48, 1677), based on parameters from NOD and Balb/c experimental data. We show that the original Copenhagen model fails to explain observed phenomena within a reasonable range of parameter values, predicting an unrealistic all-or-none disease occurrence for both strains. However, if we take into account that, in general, activated macrophages produce harmful cytokines only when engulfing necrotic (but not apoptotic) cells, then the revised model becomes qualitatively and quantitatively reasonable. Further, we show that known differences between NOD and Balb/c mouse macrophage kinetics are large enough to account for the fact that an apoptotic wave can trigger escalating inflammatory response in NOD, but not Balb/c mice. In Balb/c mice, macrophages clear the apoptotic wave so efficiently, that chronic inflammation is prevented.
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
For more information see the terms of use.
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
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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.
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