Evidence map›Paper›PMID 29515040›Full record

ArticleJCI insight2018

A peripheral blood transcriptomic signature predicts autoantibody development in infants at risk of type 1 diabetes.

Ahmed M Mehdi, Emma E Hamilton-Williams, Alexandre Cristino, Anette Ziegler, Ezio Bonifacio, Kim-Anh Le Cao, Mark Harris, Ranjeny Thomas

Open access · goldAbstract readVideo-Audio Media
In one paragraph

Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 14% of its field
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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

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  10. ZNF714 Supports Pro-Oncogenic Features in Lung Cancer Cells.International journal of molecular sciences · 2023
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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

8 authors at 3 institutions in 2 countries.

Ahmed M MehdiThe University of Queensland Diamantina Institute, Faculty of Medicine, The University of Queensland, Translational Research Institute, Woolloongabba, Australia.
Emma E Hamilton-WilliamsThe University of Queensland Diamantina Institute, Faculty of Medicine, The University of Queensland, Translational Research Institute, Woolloongabba, Australia.
Alexandre CristinoThe University of Queensland Diamantina Institute, Faculty of Medicine, The University of Queensland, Translational Research Institute, Woolloongabba, Australia.
Anette ZieglerInstitute of Diabetes Research, Helmholtz Zentrum Munchen, Neuherberg, and Forschergruppe Diabetes, Klinikum rechts der Isar, Institut für Diabetesforschung, Neuherberg, Germany.
Ezio BonifacioCRTD-DFG Research Center for Regenerative Therapies Dresden, Medical Faculty Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Kim-Anh Le CaoThe University of Queensland Diamantina Institute, Faculty of Medicine, The University of Queensland, Translational Research Institute, Woolloongabba, Australia.
Mark HarrisThe University of Queensland Diamantina Institute, Faculty of Medicine, The University of Queensland, Translational Research Institute, Woolloongabba, Australia.
Ranjeny ThomasThe University of Queensland Diamantina Institute, Faculty of Medicine, The University of Queensland, Translational Research Institute, Woolloongabba, Australia.
Translational Research Institute · AUGerman Center for Diabetes Research · DEUniversity Hospital Carl Gustav Carus · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune-mediated destruction of pancreatic islet β cells results in type 1 diabetes (T1D). Serum islet autoantibodies usually develop in genetically susceptible individuals in early childhood before T1D onset, with multiple islet autoantibodies predicting diabetes development. However, most at-risk children remain islet-antibody negative, and no test currently identifies those likely to seroconvert. We sought a genomic signature predicting seroconversion risk by integrating longitudinal peripheral blood gene expression profiles collected in high-risk children included in the BABYDIET and DIPP cohorts, of whom 50 seroconverted. Subjects were followed for 10 years to determine time of seroconversion. Any cohort effect and the time of seroconversion were corrected to uncover genes differentially expressed (DE) in seroconverting children. Gene expression signatures associated with seroconversion were evident during the first year of life, with 67 DE genes identified in seroconverting children relative to those remaining antibody negative. These genes contribute to T cell-, DC-, and B cell-related immune responses. Near-birth expression of ADCY9, PTCH1, MEX3B, IL15RA, ZNF714, TENM1, and PLEKHA5, along with HLA risk score predicted seroconversion (AUC 0.85). The ubiquitin-proteasome pathway linked DE genes and T1D susceptibility genes. Therefore, a gene expression signature in infancy predicts risk of seroconversion. Ubiquitination may play a mechanistic role in diabetes progression.

Indexed as

AutoantibodiesChild, PreschoolDiabetes Mellitus, Type 1Disease ProgressionFemaleFollow-Up StudiesGene Expression ProfilingGene Expression RegulationHumansInfantInfant, NewbornLongitudinal StudiesMalePrognosisSeroconversionTranscriptomeAutoantibodiesAutoimmune diseasesDiabetesEndocrinologyImmunology

Identifiers

PMID29515040
PMCPMC5922278
OpenAlexW2789892747

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.