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Annals of the Rheumatic Diseases 2009;68:1230-1232; doi:10.1136/ard.2008.099275
Copyright © 2009 BMJ Publishing Group Ltd & European League Against Rheumatism.

IL23R and IL12B genes: susceptibility analysis in rheumatoid arthritis

J Varade1, J Ramón Lamas2, L Rodríguez2, M Fernández-Arquero1, E Loza-Santamaría2, J Á Jover2, E G de la Concha1, B Fernández-Gutierrez2, E Urcelay1, A Martínez1

1 Immunology Department, Hospital Clínico San Carlos, Madrid, Spain
2 Rheumatology Department, Hospital Clínico San Carlos, Madrid, Spain

Correspondence to:
Dr J Varadé, Immunology Department, Hospital Universitario Clínico San Carlos, Prof Martin Lagos s/n, 28040 Madrid, Spain; gezabelvarade@gmail.com

Accepted 29 September 2008

The first 150 words of the full text of this article appear below.

The identification of additional genetic risk factors is an ongoing process that will aid in the understanding of rheumatoid arthritis (RA) aetiology. A genome-wide association scan in Crohn’s disease highlighted the IL23R gene as a susceptibility factor.1 The IL-23 receptor is a heterodimer formed by the products of two different genes: IL23R and IL12RB. Our aim was to analyse whether polymorphisms within the genes coding for the specific chain of the IL-23 receptor (IL23R) and for its p40 ligand (IL12B) and interacting in psoriasis2 are also associated with an altered risk of RA.

In agreement with previously published data,36 no statistically significant association was found with the IL12B polymorphisms (table 1).


 

The minor alleles of the IL23R polymorphisms were associated with increased predisposition to RA (table 1). . . . [Full text of this article]


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