Evidence map›Paper›PMID 18367670›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2008

The lack of anti-idiotypic antibodies, not the presence of the corresponding autoantibodies to glutamate decarboxylase, defines type 1 diabetes.

Shilpa Oak, Lisa K Gilliam, Mona Landin-Olsson, Carina Törn, Ingrid Kockum, Christina R Pennington, Merrill J Rowley, Michael R Christie, J Paul Banga, Christiane S Hampe

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.5field-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

34 citing papers in PubMed, 79 citations in OpenAlex.

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  13. DPD epitope-specific glutamic acid decarboxylase (GAD)65 autoantibodies in children with Type 1 diabetes.Diabetic medicine : a journal of the British Diabetic Association · 2017
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  14. B-CD8Journal of immunology research · 2017
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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 5 institutions in 4 countries.

Shilpa OakDepartment of Medicine, University of Washington, HSB-165, 1959 Pacific Street NE, Seattle, WA 98195, USA.
Lisa K Gilliam
Mona Landin-Olsson
Carina Törn
Ingrid Kockum
Christina R Pennington
Merrill J Rowley
Michael R Christie
J Paul Banga
Christiane S Hampe
University of Washington · USKing's College London · GBLund University · SEKarolinska Institutet · SEMonash University · AU

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Karin E Bornfeldt · 1986 to 2026
$41.4M
IMPROVING PREDICTION OF IDDMR01DK053456 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HERMAN, MARK A, REDONDO, MARIA JOSE · 1999 to 2021
$9.5M
PATHOGENESIS OF TYPE 1.5 DIABETES IN THE GENERAL POPULATIONP01DK053004 · NIDDK · UNIVERSITY OF WASHINGTON · PI LERNMARK, AKE · 1998 to 2007
$5.3M
ISLET CELL MEMBRANE ANTIBODIES IN DIABTESR01DK026190 · NIDDK · UNIVERSITY OF WASHINGTON · PI HAMPE, CHRISTIANE S · 1986 to 2016
$4.9M
NIDDK NIH HHS DK17047NIDDK NIH HHS DK26190NIDDK NIH HHS DK53004NIDDK NIH HHS DK53456NIDDK NIH HHS P01 DK053004NIDDK NIH HHS P30 DK017047NIDDK NIH HHS R01 DK026190NIDDK NIH HHS R01 DK053456
6 · The paper itself

Abstract

Autoantibodies to glutamate decarboxylase 65 (GAD65Ab) are commonly believed to be a major characteristic for type 1 diabetes (T1D). We investigated the presence of GAD65Ab in healthy individuals (n = 238) and first-degree relatives (FDRs) of T1D patients (n = 27) who tested negative for GAD65Ab in conventional RIAs. Sera were applied to affinity columns coated with GAD65-specific mAbs to absorb anti-idiotypic antibodies (anti-Ids). The absorbed sera were analyzed for binding to GAD65 by RIAs. Both healthy individuals and FDRs present GAD65Ab that are inhibited by anti-Id, masking them in conventional detection methods. The presence of GAD65Ab-specific anti-Ids was confirmed by competitive ELISA. Remarkably, T1D patients (n = 54) and Stiff Person Syndrome patients (n = 8) show a specific lack of anti-Ids to disease-associated GAD65Ab epitopes. Purified anti-Ids from healthy individuals and FDRs inhibited the binding of GAD65Ab from T1D patients to GAD65. We conclude that masked GAD65Ab are present in the healthy population and that a lack of particular anti-Ids, rather than GAD65Ab per se, is a characteristic of T1D. The lack of these inhibitory antibodies may contribute to T cell activation by GAD65Ab.

Indexed as

Antibodies, Anti-IdiotypicAutoantibodiesCase-Control StudiesDiabetes Mellitus, Type 1Family HealthGlutamate DecarboxylaseHumansRadioimmunoassayStiff-Person SyndromeAntibodies, Anti-IdiotypicAutoantibodiesGlutamate Decarboxylase

Identifiers

PMID18367670
PMCPMC2291139
OpenAlexW2127510160

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.