Evidence map›Paper›PMID 9153283›Full record

ArticleThe Journal of clinical investigation1997

Identification of naturally processed T cell epitopes from glutamic acid decarboxylase presented in the context of HLA-DR alleles by T lymphocytes of recent onset IDDM patients.

J Endl, H Otto, G Jung, B Dreisbusch, F Donie, P Stahl, R Elbracht, G Schmitz, E Meinl, M Hummel and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
7.9field-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

31 citing papers in PubMed, 147 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Antigen-specific therapeutic approaches in Type 1 diabetes.Cold Spring Harbor perspectives in medicine · 2012
    Review
  5. Molecular mimicry as a mechanism of autoimmune disease.Clinical reviews in allergy & immunology · 2012
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. 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
  11. Review
  12. Article
  13. T-cell epitopes in type 1 diabetes.Current diabetes reports · 2004
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. DR, DQ, and you: MHC alleles and autoimmunity.The Journal of clinical investigation · 2001
    Review
  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

13 authors at 6 institutions in 2 countries.

J EndlBoehringer Mannheim Research Center, D-82377 Penzberg. josef_endl@bmg.corange.com
H Otto
G Jung
B Dreisbusch
F Donie
P Stahl
R Elbracht
G Schmitz
E Meinl
M Hummel
A G Ziegler
R Wank
D J Schendel
Roche (United States) · USMünchen Klinik Schwabing · DEUniversity of Regensburg · DEUniversity of Tübingen · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DELudwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glutamic acid decarboxylase (GAD) has been defined as a major target antigen in insulin-dependent diabetes mellitus (IDDM). To identify the molecular ligands triggering a T cell response to GAD, a panel of human GAD65-specific T lymphocyte lines was generated from peripheral blood of three recent onset IDDM patients. All lines derived from a patient expressing the high-risk-conferring HLA-DR*0301/ *0401 haplotypes recognized a single epitope localized between amino acid positions 270 and 283 of GAD65, a stretch that is located in close proximity to the homology region shared with Coxsackie virus P2-C protein. All lines with this specificity were restricted to the DRA, B1*0401 product of the DR4 haplotype. Analysis of the GAD-specific T cell response in a second patient homozygous for DR4 haplotypes demonstrated that the same DRA, B1*0401 allele selected T cells specific for a different determinant. The T cell response profile in a third patient showed that DR*1501/ *1601-encoding haplotypes could present at least three different epitopes to GAD65-specific T lymphocytes. One of these epitopes was presented by a DR allele associated with the resistance-conferring DRB1*1501 haplotype. GAD-specific T cell lines could not be isolated from HLA class II-matched normal individuals. Our data reveal that (a) the T cell response to GAD65 is quite heterogenous in recent onset IDDM patients; (b) HLA-DR, not DQ, seems to be the principal restriction element used by T cells present at the onset of the disease; and (c) T cells responding to epitopes containing identical sequences to Coxsackie virus P2-C protein were not detected.

Indexed as

AllelesAmino Acid SequenceAntibodies, MonoclonalAntigen-Presenting CellsCell LineCells, CulturedCerebellumDiabetes Mellitus, Type 1EpitopesGlutamate DecarboxylaseHaplotypesHLA-DR AntigensHumansInterferon-gammaInterleukin-2Interleukin-4Antibodies, MonoclonalEpitopesGlutamate DecarboxylaseHLA-DR AntigensInterferon-gammaInterleukin-2Interleukin-4Interleukin-6

Identifiers

PMID9153283
PMCPMC508080
OpenAlexW2007341485

What OpenQuestion holds

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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.