Evidence map›Paper›PMID 20445565›Full record

ArticleGenes and immunity2010

The association between the PTPN22 1858C>T variant and type 1 diabetes depends on HLA risk and GAD65 autoantibodies.

M Maziarz, M Janer, J C Roach, W Hagopian, J P Palmer, K Deutsch, C B Sanjeevi, I Kockum, N Breslow, A Lernmark and 2 more

Open access · greenAbstract read
In one paragraph

Article in Genes and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

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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

12 authors at 6 institutions in 2 countries.

M MaziarzDepartment of Biostatistics, University of Washington, Seattle, WA 98195-7232, USA. marlenam@u.washington.edu
M Janer
J C Roach
W Hagopian
J P Palmer
K Deutsch
C B Sanjeevi
I Kockum
N Breslow
A Lernmark
Swedish Childhood Diabetes Register
Diabetes Incidence in Sweden Study Group
University of Washington · USKarolinska Institutet · SESeattle University · USCancer Research And Biostatistics · USInstitute for Systems Biology · USPacific Northwest Diabetes Research Institute · US

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Karin E Bornfeldt · 1986 to 2026
$41.4M
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 5 P30 DK17047NIDDK NIH HHS DK053004NIDDK NIH HHS DK26910NIDDK NIH HHS DK53004NIDDK NIH HHS P01 DK053004NIDDK NIH HHS P30 DK017047NIDDK NIH HHS R01 DK026190
6 · The paper itself

Abstract

The single nucleotide polymorphism 1858C>T in the PTPN22 gene is associated with type 1 diabetes (T1D) in several populations. Earlier reports have suggested that the association may be modified by human leukocyte antigen (HLA), as well as by islet autoantibodies. In a large case-control study of Swedish incident T1D patients and controls, 0-34 years of age, we tested whether the odds ratio (OR) measure of association was dependent on HLA or autoantibodies against the islet autoantigens glutamic acid decarboxylase 65 kDa autoantibodies (GADA), insulin, islet antigen-2, or islet cell. The association between the carrier status of 1858C>T allele in PTPN22 (PTPN22(CT+TT)) and T1D was modified by HLA. In addition, in GADA-positive T1D, the OR was 2.83 (2.00, 3.99), whereas in GADA-negative T1D, the OR was 1.41 (0.98, 2.04) (P for comparison=0.007). The OR of association between PTPN22(CT+TT) and GADA-positive T1D declined with increasing HLA-risk category from 6.12 to 1.54 (P=0.003); no such change was detected in GADA-negative T1D (P=0.722) (P for comparison=0.001). However, the absolute difference in risk between PTPN22(CC) and PTPN22(CT+TT) subjects with high-risk HLA was five times higher than that for subjects with low-risk HLA. We hypothesize that the altered T-cell function because of the PTPN22(1858C>T) polymorphism is exclusively associated with GADA-positive T1D at diagnosis.

Indexed as

AdolescentAdultAge FactorsAutoantibodiesCase-Control StudiesChildChild, PreschoolDiabetes Mellitus, Type 1FemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyGenotypeGlutamate DecarboxylaseHLA AntigensHumansInfantAutoantibodiesGlutamate Decarboxylaseglutamate decarboxylase 2HLA AntigensProtein Tyrosine Phosphatase, Non-Receptor Type 22PTPN22 protein, human

Identifiers

PMID20445565
PMCPMC3045194
OpenAlexW2039414380

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.