Evidence map›Paper›PMID 18576312›Full record

ArticleArthritis and rheumatism2008

A broad analysis of IL1 polymorphism and rheumatoid arthritis.

Alyssa K Johnsen, Robert M Plenge, Vincent Butty, Christopher Campbell, Rebeca Dieguez-Gonzalez, Juan J Gomez-Reino, Nancy Shadick, Michael Weinblatt, Antonio Gonzalez, Peter K Gregersen and 2 more

Abstract read
In one paragraph

Article in Arthritis and rheumatism, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 3 pooled it
1.9field-weighted citation impact, top 15% 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, 3 syntheses or guidelines pooled it, 33 citations in OpenAlex.

  1. Pooled it
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  4. Trial
  5. Association of theBiology of sport · 2024
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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 5 institutions in 2 countries.

Alyssa K JohnsenJoslin Diabetes Center, Harvard Medical School, Boston, Massachusetts, USA.
Robert M Plenge
Vincent Butty
Christopher Campbell
Rebeca Dieguez-Gonzalez
Juan J Gomez-Reino
Nancy Shadick
Michael Weinblatt
Antonio Gonzalez
Peter K Gregersen
Christophe Benoist
Diane Mathis
Brigham and Women's Hospital · USComplejo Hospitalario Universitario de Santiago · ESHarvard University · USFeinstein Institute for Medical Research · USJoslin Diabetes Center · US

Funding

MECHANISMS OF ARTHRITIC &DERMATOLOGY DISORDERST32AR007530 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI Michael B. Brenner, Ellen M Gravallese · 1986 to 2026
$10.4M
ARTHRITOGENIC IGS--WHAT ARE THEY? WHY ARE THEY MADE?R01AR046580 · NIAMS · JOSLIN DIABETES CENTER · PI MATHIS, DIANE J · 2000 to 2009
$3.8M
Genetic Control of IL-1 and its Role in Inflammatory ArthritisK08AI072044 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI JOHNSEN, ALYSSA K. · 2007 to 2010
$520k
NIAID NIH HHS K08 AI072044NIAID NIH HHS K08-AI-072044-01A1NIAMS NIH HHS R01 AR046580NIAMS NIH HHS R01-AR-046580-08NIAMS NIH HHS T32 AR007530NIAMS NIH HHS T32-AR-007530-21
6 · The paper itself

Abstract

objectiveIt has been suggested that polymorphisms in IL1 are correlated with severe and/or erosive rheumatoid arthritis (RA), but the implicated alleles have differed among studies. The aim of this study was to perform a broad and well-powered search for association between allelic polymorphism in IL1A and IL1B and the susceptibility to or severity of RA.

methodsKey coding and regulatory regions in IL1A and IL1B were sequenced in 24 patients with RA, revealing 4 novel single-nucleotide polymorphisms (SNPs) in IL1B. These and a comprehensive set of 24 SNPs tagging most of the underlying genetic diversity were genotyped in 3 independent RA case-control sample sets and 1 longitudinal RA cohort, totaling 3,561 patients and 3,062 control subjects.

resultsNo fully significant associations were observed. Analysis of the discovery case-control sample sets indicated a potential association of IL1B promoter region SNPs with susceptibility to RA (for RA3/A, odds ratio [OR] 1.27, P = 0.0021) or with the incidence of radiographic erosions (for RA4/C, OR 1.56, P = 0.036), but these findings were not replicated in independent case-control samples. No association with rheumatoid factor, anti-cyclic citrullinated peptide, or the Disease Activity Score in 28 joints was found. None of the associations previously observed in other studies were replicated here.

conclusionIn spite of a broad and highly powered study, we observed no robust, reproducible association between IL1A/B variants and the susceptibility to or severity of RA in white individuals of European descent. Our results provide evidence that, in the majority of cases, polymorphism in IL1A and IL1B is not a major contributor to genetic susceptibility to RA.

Indexed as

Polymorphism, Single NucleotideAdolescentAdultArthritis, RheumatoidCase-Control StudiesFemaleGenetic Predisposition to DiseaseHaplotypesHumansInterleukin-1alphaInterleukin-1betaMaleMiddle AgedSeverity of Illness IndexIL1A protein, humanIL1B protein, humanInterleukin-1alphaInterleukin-1beta

Identifiers

PMID18576312
PMCPMC2533126
OpenAlexW2056018046

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.