Evidence map›Paper›PMID 17641683›Full record

ArticleGenes and immunity2007

IA-2 autoantibodies in incident type I diabetes patients are associated with a polyadenylation signal polymorphism in GIMAP5.

J-H Shin, M Janer, B McNeney, S Blay, K Deutsch, C B Sanjeevi, I Kockum, A Lernmark, J Graham, Swedish Childhood Diabetes Study Group and 40 more

Abstract read
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In one paragraph

Article in Genes and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 44 citations in OpenAlex.

  1. Quantitative temporal analysis of pancreatic islet T lymphocyte and macrophage infiltration heralded by serum IgE in congenic BioBreeding (BB) Gimap5Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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  6. Loss of GTPase of immunity-associated protein 5 (Gimap5) promotes pathogenic CD4The Journal of allergy and clinical immunology · 2019
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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

50 authors at 4 institutions in 3 countries.

J-H ShinDepartment of Statistics and Actuarial Science, Simon Fraser University, Burnaby, British Columbia, Canada.
M Janer
B McNeney
S Blay
K Deutsch
C B Sanjeevi
I Kockum
A Lernmark
J Graham
Swedish Childhood Diabetes Study Group
Diabetes Incidence in Sweden Study Group
Hans Arnqvist
Elizabeth Björck
Jan Eriksson
Lennarth Nyström
Lars Olof Ohlson
Bengt Scherstén
Jan Ostman
M Aili
L E Bååth
E Carlsson
H Edenwall
G Forsander
B W Granström
I Gustavsson
R Hanås
L Hellenberg
H Hellgren
E Holmberg
H Hörnell
Sten-A Ivarsson
C Johansson
G Jonsell
K Kockum
B Lindblad
A Lindh
J Ludvigsson
U Myrdal
J Neiderud
K Segnestam
S Sjöblad
L Skogsberg
L Strömberg
U Ståhle
B Thalme
K Tullus
T Tuvemo
M Wallensteen
O Westphal
J Aman
Simon Fraser University · CAKarolinska Institutet · SESeattle University · USInstitute for Systems Biology · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In a large case-control study of Swedish incident type I diabetes patients and controls, 0-34 years of age, we tested the hypothesis that the GIMAP5 gene, a key genetic factor for lymphopenia in spontaneous BioBreeding rat diabetes, is associated with type I diabetes; with islet autoantibodies in incident type I diabetes patients or with age at clinical onset in incident type I diabetes patients. Initial scans of allelic association were followed by more detailed logistic regression modeling that adjusted for known type I diabetes risk factors and potential confounding variables. The single nucleotide polymorphism (SNP) rs6598, located in a polyadenylation signal of GIMAP5, was associated with the presence of significant levels of IA-2 autoantibodies in the type I diabetes patients. Patients with the minor allele A of rs6598 had an increased prevalence of IA-2 autoantibody levels compared to patients without the minor allele (OR=2.2; Bonferroni-corrected P=0.003), after adjusting for age at clinical onset (P=8.0 x 10(-13)) and the numbers of HLA-DQ A1*0501-B1*0201 haplotypes (P=2.4 x 10(-5)) and DQ A1*0301-B1*0302 haplotypes (P=0.002). GIMAP5 polymorphism was not associated with type I diabetes or with GAD65 or insulin autoantibodies, ICA, or age at clinical onset in patients. These data suggest that the GIMAP5 gene is associated with islet autoimmunity in type I diabetes and add to recent findings implicating the same SNP in another autoimmune disease.

Indexed as

AdolescentAdultAutoantibodiesCase-Control StudiesChildChild, PreschoolDiabetes Mellitus, Type 1FemaleGTP-Binding ProteinsHumansInfantInfant, NewbornMalePolymorphism, Single NucleotideSwedenAutoantibodiesGIMAP5 protein, humanGTP-Binding ProteinsICA512 autoantibody

Identifiers

PMID17641683
OpenAlexW2001242651

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.