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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)

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

PROVIDER: PRJNA1013949 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25940268.fastq.gz	Fastqsanger.gz
	SRR25940269.fastq.gz	Fastqsanger.gz
	SRR25940270.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 EVs)

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.

2024-05-24 | GSE242565 | GEO

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

2024-05-24 | GSE242567 | GEO

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

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

| PRJNA1013951 | ENA

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

2024-05-24 | GSE242561 | GEO

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

2024-05-24 | GSE242566 | GEO

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

2024-05-24 | GSE242564 | GEO

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

2024-05-24 | GSE242563 | GEO

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

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

| PRJNA1013941 | ENA

tRNA-derived fragments in T lymphocyte-beta cell crosstalk and in type 1 diabetes pathogenesis in NOD mice.

Project description: Not available

| S-EPMC11446995 | biostudies-literature

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.

2024-05-14 | GSE256343 | GEO

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