Evidence map›Paper›PMID 31127054›Full record

ReviewDiabetes2019

NIH Initiative to Improve Understanding of the Pancreas, Islet, and Autoimmunity in Type 1 Diabetes: The Human Pancreas Analysis Program (HPAP).

Klaus H Kaestner, Alvin C Powers, Ali Naji, HPAP Consortium, Mark A Atkinson

Open access · bronzeAbstract readReview
In one paragraph

Review in Diabetes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
149citing papers in PubMed, 1 pooled it
9.3field-weighted citation impact, top 2% 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

149 citing papers in PubMed, 1 synthesis or guideline pooled it, 169 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. mNature metabolism · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. Spatium: A Protein Language Foundation Model for Spatial Proteomics.bioRxiv : the preprint server for biology · 2026
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. A surviving beta cell subpopulation enriched in patients with T1D.bioRxiv : the preprint server for biology · 2026
    Article
  19. Article
  20. Article

89 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 1 country.

Klaus H KaestnerDepartment of Genetics and Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA kaestner@pennmedicine.upenn.edu.ORCID 0000-0002-1228-021X
Alvin C PowersDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN.ORCID 0000-0003-1941-5786
Ali NajiDepartment of Surgery, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
HPAP Consortium
Mark A AtkinsonDepartments of Pathology and Pediatrics, University of Florida Diabetes Institute, Gainesville, FL.
University of Pennsylvania · USUniversity of Florida · USVanderbilt University · US

Funding

Penn integrated Human Pancreas procurement and Analysis ProgramUC4DK112217 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI BETTS, MICHAEL R, FELDMAN, MICHAEL D · 2016 to 2020
$17.8M
Supplement to Integrated Program for Human Pancreas Procurement and AnalysisUC4DK112232 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI ATKINSON, MARK A., POWERS, ALVIN C · 2016 to 2020
$8.4M
NIDDK NIH HHS UC4 DK112217NIDDK NIH HHS UC4 DK112232
6 · The paper itself

Abstract

Type 1 diabetes risk can reliably be predicted by markers of autoimmunity, but approaches to prevent or modify the underlying disease process are needed. We posit this void fundamentally results from a limited understanding of immune-islet cell interactions within the pancreas and relevant immune organs, contributions of β-cells to their own demise, and epigenetic predispositions affecting both immune and islet cells. Because biopsy of the human pancreas and pancreatic lymph nodes carries risk and the pancreas begins to autodigest soon after death, detailed cellular and molecular phenotyping of the human type 1 diabetes pancreas is lacking, limiting our understanding of the mechanisms of β-cell loss. To address these challenges, the National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases established the Human Pancreas Analysis Program (HPAP) to procure human type 1 diabetes pancreata for an extensive array of tissue-based, cellular, and epigenetic assays aimed at critical knowledge gaps in our understanding of the local immune attack and loss of β-cells. In this Methodology Review, we describe how HPAP is performing detailed islet and immune cell phenotyping and creating publicly available data sets with the goals of an improved understanding of type 1 diabetes and the development of more effective treatments to prevent or reverse the disease.

Indexed as

AutoimmunityDiabetes Mellitus, Type 1HumansInsulinInsulin-Secreting CellsNational Institutes of Health (U.S.)PancreasUnited StatesInsulin

Identifiers

PMID31127054
PMCPMC6609987
OpenAlexW2945198601

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.