Evidence map›Paper›PMID 35881836›Full record

ReviewDiabetes2022

The β-Cell in Type 1 Diabetes Pathogenesis: A Victim of Circumstances or an Instigator of Tragic Events?

Roberto Mallone, Clémentine Halliez, Jinxiu Rui, Kevan C Herold

Open access · bronzeAbstract readReview
In one paragraph

Review in Diabetes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Type 1 Diabetes Mellitus Pathogenesis: Mechanisms, Early Diagnostic Strategies, and Emerging Therapeutic Approaches.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. IFN-α Induces Heterogenous ROS Production in Human β-Cells.bioRxiv : the preprint server for biology · 2025
    Article
  19. Article
  20. Review
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

4 authors at 2 institutions in 2 countries.

Roberto MalloneUniversité Paris Cité, Institut Cochin, CNRS, INSERM, Paris, France.ORCID 0000-0002-9846-8861
Clémentine HalliezUniversité Paris Cité, Institut Cochin, CNRS, INSERM, Paris, France.
Jinxiu RuiDepartments of Immunobiology and Internal Medicine, Yale University, New Haven, CT.
Kevan C HeroldDepartments of Immunobiology and Internal Medicine, Yale University, New Haven, CT.ORCID 0000-0003-1534-6613
Centre National de la Recherche Scientifique · FRYale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Yale Diabetes Research CenterP30DK045735 · NIDDK · YALE UNIVERSITY · PI Richard A Flavell · 1993 to 2026
$44.0M
Phase II Trial of HOKT3gamma 1 (ALA-ALA) in Type 1 DiabetesR01DK057846 · NIDDK · YALE UNIVERSITY · PI Kevan C Herold · 2000 to 2026
$11.1M
Epigenetic, Protein, and Cellular Biomarkers of Beta Cell Function in T1DUC4DK104205 · NIDDK · YALE UNIVERSITY · PI HEROLD, KEVAN C · 2014 to 2014
$2.5M
Analysis of beta cell death in Type 1 diabetesDP3DK101122 · NIDDK · YALE UNIVERSITY · PI HEROLD, KEVAN C · 2013 to 2013
$807k
Novel diagnostics for autoimmunity from checkpoint inhibitor immune therapyR43DK116577 · NIDDK · L2 DIAGNOSTICS, LLC · PI HEROLD, KEVAN C, USMANI-BROWN, SAHAR · 2017 to 2017
$300k
NCATS NIH HHS UL1 TR001863NIDDK NIH HHS DP3 DK101122NIDDK NIH HHS P30 DK045735NIDDK NIH HHS R01 DK057846NIDDK NIH HHS R43 DK116577NIDDK NIH HHS UC4 DK104205
6 · The paper itself

Abstract

Recent reports have revived interest in the active role that β-cells may play in type 1 diabetes pathogenesis at different stages of disease. In some studies, investigators suggested an initiating role and proposed that type 1 diabetes may be primarily a disease of β-cells and only secondarily a disease of autoimmunity. This scenario is possible and invites the search for environmental triggers damaging β-cells. Another major contribution of β-cells may be to amplify autoimmune vulnerability and to eventually drive it into an intrinsic, self-detrimental state that turns the T cell-mediated homicide into a β-cell suicide. On the other hand, protective mechanisms are also mounted by β-cells and may provide novel therapeutic targets to combine immunomodulatory and β-cell protective agents. This integrated view of autoimmunity as a disease of T-cell/β-cell cross talk will ultimately advance our understanding of type 1 diabetes pathogenesis and improve our chances of preventing or reversing disease progression.

Indexed as

Diabetes Mellitus, Type 1Insulin-Secreting CellsAutoimmunityHumansImmunomodulationT-Lymphocytes

Identifiers

PMID35881836
PMCPMC9490354
OpenAlexW4288032887

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.