Evidence map›Paper›PMID 22069258›Full record

ReviewDiabetes/metabolism research and reviews2011

Insulin as a key autoantigen in the development of type 1 diabetes.

Maki Nakayama

Open access · greenAbstract readReview
In one paragraph

Review in Diabetes/metabolism research and reviews, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

38 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Review
  3. Cellular therapies in rheumatic and musculoskeletal diseases.Journal of translational autoimmunity · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Activation pathways that drive CD4Immunological reviews · 2022
    Review
  12. Preclinical evaluation of a precision medicine approach to DNA vaccination in type 1 diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  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

1 author at 1 institution in 1 country.

Maki NakayamaBarbara Davis Center for Childhood Diabetes, University of Colorado Denver, Aurora, CO 80045, USA. maki.nakayama@ucdenver.edu
University of Colorado Denver · US

Funding

Virginia Mason/UCHSC Autoimmune Prevention CenterU19AI050864 · NIAID · UNIVERSITY OF COLORADO DENVER · PI HOLERS, VERNON MICHAEL · 2001 to 2011
$29.2M
UCHSC DIABETES ENDOCRINOLOGY RESEARCH CENTERP30DK057516 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI HUTTON, JOHN C · 2000 to 2010
$14.0M
STRUCTURE PEPTIDE/CONSERVED T CELL RECEPTOR DETERMINING DIABETESR00DK080885 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI NAKAYAMA, MAKI · 2010 to 2012
$742k
NIAID NIH HHS U19 AI050864NIDDK NIH HHS P30 DK057516NIDDK NIH HHS R00 DK080885
6 · The paper itself

Abstract

Type 1 diabetes is a T-cell-mediated autoimmune disease against pancreatic beta cells. T cells target various antigens such as insulin, chromogranin A, glutamic acid decarboxylase and islet-specific glucose-6-phosphatase catalytic subunit-related protein. Elimination of insulin dramatically prevents diabetes in the non-obese diabetic (NOD) mouse model and response to insulin occurs prior to that to other antigens. These findings suggest that insulin is a target antigen at the early stage of the disease and is likely to be essential to cause anti-islet autoimmunity in NOD mice. In this review, we discuss whether insulin is truly essential and is only the single essential autoantigen for NOD mice and potentially for man. Although the ultimate principle is still being addressed, it is certain that T-cell response to insulin is a major check point to develop type 1 diabetes in NOD mice. Given multiple similarities between diabetes of NOD mice and man, targeting insulin and insulin-reactive T cells may provide opportunities to develop robust immunotherapies.

Indexed as

AnimalsAutoantigensAutoimmunityDiabetes Mellitus, Type 1HumansInsulinInsulin-Secreting CellsMiceMice, Inbred NODPeptide FragmentsT-LymphocytesAutoantigensInsulininsulin B (9-23)Peptide Fragments

Identifiers

PMID22069258
PMCPMC5439426
OpenAlexW2057552502

What OpenQuestion holds

Textmetadata
LicenceTDM
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.