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Whole population RNASeq of pancreatic islet macrophages during autoimmune diabetes progression

ABSTRACT: Whole population RNASeq of pancreatic islet macrophages during autoimmune diabetes progression

PROVIDER: PRJNA594721 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10641200.fastq.gz	Fastqsanger.gz
	SRR10641201.fastq.gz	Fastqsanger.gz
	SRR10641202.fastq.gz	Fastqsanger.gz
	SRR10641125.fastq.gz	Fastqsanger.gz
	SRR10641126.fastq.gz	Fastqsanger.gz

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Whole population RNASeq of pancreatic islet macrophages during autoimmune diabetes progression

Project description:Whole population RNASeq of pancreatic islet macrophages during autoimmune diabetes progression.

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Circulating Metabolites in Progression to Islet Autoimmunity and Type 1 Diabetes

Project description:<h4><strong>AIMS/HYPOTHESIS: </strong>Metabolic dysregulation may precede the onset of type 1 diabetes. However, these metabolic disturbances and their specific role in disease initiation remain poorly understood. In this study, we examined whether children who progress to type 1 diabetes have a circulatory polar metabolite profile distinct from that of children who later progress to islet autoimmunity but not type 1 diabetes and a matched control group.</h4><h4><strong>METHODS: </strong>We analysed polar metabolites from 415 longitudinal plasma samples in a prospective cohort of children in three study groups: those who progressed to type 1 diabetes; those who seroconverted to one islet autoantibody but not to type 1 diabetes; and an antibody-negative control group. Metabolites were measured using two-dimensional GC high-speed time of flight MS.</h4><h4><strong>RESULTS: </strong>In early infancy, progression to type 1 diabetes was associated with downregulated amino acids, sugar derivatives and fatty acids, including catabolites of microbial origin, compared with the control group. Methionine remained persistently upregulated in those progressing to type 1 diabetes compared with the control group and those who seroconverted to one islet autoantibody. The appearance of islet autoantibodies was associated with decreased glutamic and aspartic acids.</h4><h4><strong>CONCLUSIONS/INTERPRETATION: </strong>Our findings suggest that children who progress to type 1 diabetes have a unique metabolic profile, which is, however, altered with the appearance of islet autoantibodies. Our findings may assist with early prediction of the disease.</h4>

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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.

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