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Role of tRNA-derived fragments in the cross-talk between immune cells and beta cells during type 1 diabetes pathogenesis (NOD islets)

ABSTRACT: Role of tRNA-derived fragments in the cross-talk between immune cells and beta cells during type 1 diabetes pathogenesis (NOD islets)

PROVIDER: PRJNA1013951 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25941100.fastq.gz	Fastqsanger.gz
	SRR25941101.fastq.gz	Fastqsanger.gz
	SRR25941102.fastq.gz	Fastqsanger.gz
	SRR25941103.fastq.gz	Fastqsanger.gz
	SRR25941104.fastq.gz	Fastqsanger.gz

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Role of tRNA-derived fragments in the cross-talk between immune cells and beta cells during type 1 diabetes pathogenesis (NOD islets)

Project description:Transfer RNAs (tRNAs) play a central and well recognized role in protein synthesis. Recent studies revealed that these molecules can be cleaved to generate tRNA fragments (tRFs) with regulatory functions. Here, we studied the contribution of tRFs to pancreatic β-cell loss during the initial phases of type 1 diabetes (T1D), an autoimmune disorder characterized by the invation of immune cells in the pancreas and progressive loss of insulin-secreting cells. Small RNA-profiling showed that the pool of tRFs present in pancreatic β-cells is altered in non-obese diabetic (NOD) mice, a mouse model used to study T1D. We found that part of these changes is triggered by the exposure of β-cells to proinflammatory cytokines released during the autoimmune reaction while others result from the direct transfer of tRFs from autoreactive T lymphocytes to insulin-secreting cells via extracellular vesicles. Indeed, using an RNA-tagging approach, we could demonstrate that a group of tRFs are transferred in vivo in from CD4+CD25- T lymphocytes to pancreatic β-cells, upon T cell adoptive transfer in NOD scid mice. Morevoer, the up-regulation of selected tRFs associated with the autoimmune reaction triggers β-cell apoptosis and gene expression changes that affect the immune regulatory capacity of β-cells. Our data point to tRFs as novel players in type 1 diabetes and potentially in other autoimmune disorders.

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Detection of the tRNA-derived fragments in human pancreatic islets of control individuals

Project description:Cytosolic and mitochondrial fragments that arise from the cleavage of tRNAs and mt-tRNAs, respectively, have been identified as potential novel regulators of cellular functions. In this study we identified hundreds of fragments in the pancreatic islets of healthy human individuals. We were able to annotate 3593 tRFs (16-55 base pairs) present in the islets of healthy human individuals (we considered a minimum of 5 cpm values in each of the 3 samples). Interestingly, the vast majority of the tRFs whose levels are altered in pancreatic islets of prediabetic NOD mice and in extracellular vesicles released by activated CD4+ T lymphocytes, are conserved in humans and were detected in human pancreatic islets. This suggests a possible conservation of the findings of this study in a human context.

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Role of tRNA-derived fragments in the cross-talk between immune cells and beta cells during type 1 diabetes pathogenesis (NOD EVs)

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Role of tRNA-derived fragments in the cross-talk between immune cells and beta cells during type 1 diabetes pathogenesis (NOD EVs)

Project description:Role of tRNA-derived fragments in the cross-talk between immune cells and beta cells during type 1 diabetes pathogenesis (NOD EVs)

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Proteomics analysis of islets of 6-week old NOR and NOD mice

Project description:Islets from 6-week old NOR and NOD mice were submitted to proteomics analysis to study differences in insulitis and type 1 diabetes development.

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Comparison of gene expression between islets from NOD-Rag and NOD-Idd22 mice

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.

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Single cell RNA-sequencing analysis of islets from WT NOD mice on different diets

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.

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Role of tRNA-derived fragments in the cross-talk between immune cells and beta cells during type 1 diabetes pathogenesis (Cyt-treated)

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