Evidence map›Paper›PMID 8529129›Full record

ArticleMolecular medicine (Cambridge, Mass.)1995

Similar peptides from two beta cell autoantigens, proinsulin and glutamic acid decarboxylase, stimulate T cells of individuals at risk for insulin-dependent diabetes.

G Rudy, N Stone, L C Harrison, P G Colman, P McNair, V Brusic, M B French, M C Honeyman, B Tait, A M Lew

Open access · greenAbstract readComparative Study
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

36 citing papers in PubMed, 102 citations in OpenAlex.

  1. Review
  2. T-Cell Receptor Sequences Identify Combined Coxsackievirus-International journal of molecular sciences · 2024
    Article
  3. International journal of molecular sciences · 2023
    Article
  4. Review
  5. An Insulin-Inspired Supramolecular Hydrogel for Prevention of Type 1 Diabetes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021
    Article
  6. Article
  7. Autoreactive T cells in type 1 diabetes.The Journal of clinical investigation · 2017
    Review
  8. Molecular mimicry: its evolution from concept to mechanism as a cause of autoimmune diseases.Monoclonal antibodies in immunodiagnosis and immunotherapy · 2014
    Article
  9. Antigen-specific therapeutic approaches in Type 1 diabetes.Cold Spring Harbor perspectives in medicine · 2012
    Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Insulin as an autoantigen in NOD/human diabetes.Current opinion in immunology · 2008
    Review
  15. Review
  16. Proinsulin is encoded by an RNA splice variant in human blood myeloid cells.Proceedings of the National Academy of Sciences of the United States of America · 2006
    Article
  17. Article
  18. Recognition of a subregion of human proinsulin by class I-restricted T cells in type 1 diabetic patients.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
  19. Article
  20. 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

10 authors at 1 institution in 1 country.

G RudyWalter and Eliza Hall Institute of Medical Research, Melbourne, Australia.
N Stone
L C Harrison
P G Colman
P McNair
V Brusic
M B French
M C Honeyman
B Tait
A M Lew
Walter and Eliza Hall Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInsulin (1) and glutamic acid decarboxylase (GAD) (2) are both autoantigens in insulin-dependent diabetes mellitus (IDDM), but no molecular mechanism has been proposed for their association. We have identified a 13 amino acid peptide of proinsulin (amino acids 24-36) that bears marked similarity to a peptide of GAD65 (amino acids 506-518) (G. Rudy, unpublished). In order to test the hypothesis that this region of similarity is implicated in the pathogenesis of IDDM, we assayed T cell reactivity to these two peptides in subjects at risk for IDDM. MATERIALS AND

methodsSubjects at risk for IDDM were islet cell antibody (ICA)-positive, first degree relatives of people with insulin-dependent diabetes. Peripheral blood mononuclear cells from 10 pairs of at-risk and HLA-DR matched control subjects were tested in an in vitro proliferation assay.

resultsReactivity to both proinsulin and GAD peptides was significantly greater among at-risk subjects than controls (proinsulin; p < 0.008; GAD; p < 0.018). In contrast to reactivity to the GAD peptide, reactivity to the proinsulin peptide was almost entirely confined to the at-risk subjects.

conclusionsThis is the first demonstration of T cell reactivity to a proinsulin-specific peptide. In addition, it is the first example of reactivity to a minimal peptide region shared between two human autoimmune disease-associated self antigens. Mimicry between these similar peptides may provide a molecular basis for the conjoint autoantigenicity of proinsulin and GAD in IDDM.

Indexed as

AdolescentAdultAmino Acid SequenceAnimalsAutoantibodiesAutoantigensChildDiabetes Mellitus, Type 1Glutamate DecarboxylaseHumansIslets of LangerhansLymphocyte ActivationMiceMolecular Sequence DataPeptide FragmentsPrediabetic StateAutoantibodiesAutoantigensGlutamate Decarboxylaseislet cell antibodyPeptide FragmentsProinsulin

Identifiers

PMID8529129
PMCPMC2229979
OpenAlexW83554749

What OpenQuestion holds

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Registered trials

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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.