Evidence map›Paper›PMID 31671072›Full record

ArticleJCI insight2019

A composite immune signature parallels disease progression across T1D subjects.

Cate Speake, Samuel O Skinner, Dror Berel, Elizabeth Whalen, Matthew J Dufort, William Chad Young, Jared M Odegard, Anne M Pesenacker, Frans K Gorus, Eddie A James and 8 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Trial
  2. Article
  3. Time to reframe the disease staging system for type 1 diabetes.The lancet. Diabetes & endocrinology · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Endotypes in T1D: B lymphocytes and early onset.Current opinion in endocrinology, diabetes, and obesity · 2020
    Review
  13. Article
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

18 authors at 7 institutions in 3 countries.

Cate SpeakeBenaroya Research Institute at Virginia Mason, Seattle, Washington, USA.
Samuel O SkinnerBenaroya Research Institute at Virginia Mason, Seattle, Washington, USA.
Dror BerelVaccines and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.
Elizabeth WhalenBenaroya Research Institute at Virginia Mason, Seattle, Washington, USA.
Matthew J DufortBenaroya Research Institute at Virginia Mason, Seattle, Washington, USA.
William Chad YoungVaccines and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.
Jared M OdegardBenaroya Research Institute at Virginia Mason, Seattle, Washington, USA.
Anne M PesenackerUniversity of British Columbia BC Children's Hospital Research Institute, Vancouver, British Columbia, Canada.
Frans K GorusDiabetes Research Center, Medical School and University Hospital (UZ Brussel), Brussels Free University Vrije Universiteit Brussel, Brussels, Belgium.
Eddie A JamesBenaroya Research Institute at Virginia Mason, Seattle, Washington, USA.
Megan K LevingsUniversity of British Columbia BC Children's Hospital Research Institute, Vancouver, British Columbia, Canada.
Peter S LinsleyBenaroya Research Institute at Virginia Mason, Seattle, Washington, USA.
Eitan M AkiravResearch Institute, Islet Biology, New York University Winthrop Hospital, Mineola, New York, USA.
Alberto PuglieseDiabetes Research Institute, Department of Medicine, Division of Diabetes Endocrinology and Metabolism, Department of Microbiology and Immunology, Miller School of Medicine, University of Miami, Miami, Florida, USA.
Martin J HessnerMedical College of Wisconsin, Milwaukee, Wisconsin, USA.
Gerald T NepomBenaroya Research Institute at Virginia Mason, Seattle, Washington, USA.
Raphael GottardoVaccines and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.
S Alice LongBenaroya Research Institute at Virginia Mason, Seattle, Washington, USA.
Virginia Mason Medical Center · USInfectious Disease Research Institute · USBC Children's Hospital · CAMedical College of Wisconsin · USUniversity of Miami · USVrije Universiteit Brussel · BEWinthrop-University Hospital · US

Funding

Immune Tolerance Network UM1 2023 SupplementUM1AI109565 · NIAID · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI Mark S Anderson, Jane Hoyt Buckner · 2014 to 2026
$451.6M
Determining the molecular basis for different rates of T1D progressionDP3DK104465 · NIDDK · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI LINSLEY, PETER S · 2014 to 2014
$1.1M
NIAID NIH HHS UM1 AI109565NIDDK NIH HHS DP3 DK104465Versus Arthritis 21738
6 · The paper itself

Abstract

At diagnosis, most people with type 1 diabetes (T1D) produce measurable levels of endogenous insulin, but the rate at which insulin secretion declines is heterogeneous. To explain this heterogeneity, we sought to identify a composite signature predictive of insulin secretion, using a collaborative assay evaluation and analysis pipeline that incorporated multiple cellular and serum measures reflecting β cell health and immune system activity. The ability to predict decline in insulin secretion would be useful for patient stratification for clinical trial enrollment or therapeutic selection. Analytes from 12 qualified assays were measured in shared samples from subjects newly diagnosed with T1D. We developed a computational tool (DIFAcTO, Data Integration Flexible to Account for different Types of data and Outcomes) to identify a composite panel associated with decline in insulin secretion over 2 years following diagnosis. DIFAcTO uses multiple filtering steps to reduce data dimensionality, incorporates error estimation techniques including cross-validation and sensitivity analysis, and is flexible to assay type, clinical outcome, and disease setting. Using this novel analytical tool, we identified a panel of immune markers that, in combination, are highly associated with loss of insulin secretion. The methods used here represent a potentially novel process for identifying combined immune signatures that predict outcomes relevant for complex and heterogeneous diseases like T1D.

Indexed as

Disease ProgressionAdolescentAdultChildComputational BiologyDiabetes Mellitus, Type 1FemaleHumansHypoglycemic AgentsImmunotherapyInsulin-Secreting CellsInsulin SecretionMaleYoung AdultHypoglycemic AgentsAutoimmunityDiabetesImmunotherapyMolecular pathology

Identifiers

PMID31671072
PMCPMC6962023
OpenAlexW2983993007

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.