Evidence map›Paper›PMID 38967669›Full record

ArticleDiabetologia2024

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

Flora Brozzi, Cécile Jacovetti, Cristina Cosentino, Véronique Menoud, Kejing Wu, Mustafa Bilal Bayazit, Baroj Abdulkarim, Christian Iseli, Nicolas Guex, Claudiane Guay and 1 more

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In one paragraph

Article in Diabetologia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Flora BrozziDepartment of Fundamental Neurosciences, University of Lausanne, Lausanne, Switzerland.
Cécile Jacovetti *Department of Fundamental Neurosciences, University of Lausanne, Lausanne, Switzerland.
Cristina Cosentino *Department of Fundamental Neurosciences, University of Lausanne, Lausanne, Switzerland.
Véronique MenoudDepartment of Fundamental Neurosciences, University of Lausanne, Lausanne, Switzerland.
Kejing WuDepartment of Fundamental Neurosciences, University of Lausanne, Lausanne, Switzerland.
Mustafa Bilal BayazitDepartment of Fundamental Neurosciences, University of Lausanne, Lausanne, Switzerland.
Baroj AbdulkarimHaya Therapeutics SA, Épalinges, Switzerland.
Christian IseliBioinformatics Competence Centre, University of Lausanne, Lausanne, Switzerland.
Nicolas GuexBioinformatics Competence Centre, University of Lausanne, Lausanne, Switzerland.
Claudiane GuayDepartment of Fundamental Neurosciences, University of Lausanne, Lausanne, Switzerland.
Romano RegazziDepartment of Fundamental Neurosciences, University of Lausanne, Lausanne, Switzerland. Romano.Regazzi@unil.ch.

Funding

Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung 310030-188447Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung 310030-219252
6 · The paper itself

Abstract

aims/hypothesistRNAs play a central role in protein synthesis. Besides this canonical function, they were recently found to generate non-coding RNA fragments (tRFs) regulating different cellular activities. The aim of this study was to assess the involvement of tRFs in the crosstalk between immune cells and beta cells and to investigate their contribution to the development of type 1 diabetes.

methodsGlobal profiling of the tRFs present in pancreatic islets of 4- and 8-week-old NOD mice and in extracellular vesicles released by activated CD4

resultsWe found that the tRF pool was altered in the islets of NOD mice during the initial phases of type 1 diabetes. Part of these changes were triggered by prolonged exposure of beta cells to proinflammatory cytokines (IL-1β, TNF-α and IFN-γ) while others resulted from the delivery of tRFs produced by CD4 CONCLUSIONS/

interpretationOur data point to tRFs as novel players in the crosstalk between the immune system and insulin-secreting cells and suggest a potential involvement of this novel class of non-coding RNAs in type 1 diabetes pathogenesis. DATA AVAILABILITY: Sequences are available from the Gene Expression Omnibus (GEO) with accession numbers GSE242568 and GSE256343.

Indexed as

Diabetes Mellitus, Type 1Insulin-Secreting CellsMice, Inbred NODRNA, TransferAnimalsApoptosisCD4-Positive T-LymphocytesExtracellular VesiclesFemaleIslets of LangerhansMiceRNA, UntranslatedT-LymphocytesRNA, TransferRNA, UntranslatedApoptosisAutoimmunityExtracellular vesiclesInsulinPancreatic islet

Identifiers

PMID38967669
PMCPMC11446995

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.