Skip Navigation


Rheumatology Advance Access originally published online on August 18, 2006
Rheumatology 2007 46(3):409-411; doi:10.1093/rheumatology/kel300
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
46/3/409    most recent
kel300v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (1)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Harrison, P.
Right arrow Articles by Wordsworth, B. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Harrison, P.
Right arrow Articles by Wordsworth, B. P.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2006. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

MHC2TA promoter polymorphism (–168*G/A, rs3087456) is not associated with susceptibility to rheumatoid arthritis in British Caucasian rheumatoid arthritis patients

P. Harrison, J. J. Pointon, C. Farrar1, A. Harin1 and B. P. Wordsworth

University of Oxford Institute of Musculoskeletal Sciences, Botnar Research Centre and 1Nuffield Department of Orthopaedic Surgery Nuffield Orthopaedic Centre, Oxford, UK.

Correspondence to: Pille Harrison, Botnar Research Centre, University of Oxford, Nuffield Orthopaedic Centre, Oxford OX3 7LD, UK. E-mail: pille.harrison{at}ndos.ox.ac.uk


   Abstract

Objective. To investigate the association of a single-nucleotide polymorphism (SNP) in the promoter region of MHC2TA gene (–168*G/A, rs3087456), which has previously been described in a Swedish rheumatoid arthritis (RA) cohort, in British Caucasian RA patients.

Methods. We genotyped 733 RA patients and 613 healthy controls for MHC2TA 168*G/A SNP by amplification-refractory mutation system (ARMS). Data were analysed using SPSS version 13.0 software and the chi-square test was applied where appropriate.

Results. The MHC2TA 168*G/A SNP was not associated with increased susceptibility to RA in our patients. Stratifying the patients according to the presence or absence of rheumatoid factor (RF) showed the SNP to be more common in RF negative patients, but this did not reach statistical significance.

Conclusion. We did not confirm the previously reported association of this MHC2TA polymorphism with RA in our UK population despite its ethnic similarities with the Swedish population in which it was first described.

KEY WORDS: MHC2TA, Rheumatoid arthritis, HLA, Rheumatoid factor negative

Submitted 11 June 2006; revised version accepted 14 July 2006.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Ann Rheum DisHome page
P G Bronson, L A Criswell, and L F Barcellos
The MHC2TA -168A/G polymorphism and risk for rheumatoid arthritis: a meta-analysis of 6861 patients and 9270 controls reveals no evidence for association
Ann Rheum Dis, July 1, 2008; 67(7): 933 - 936.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
K. Harnesk, M. Swanberg, J. Ockinger, M. Diez, O. Lidman, E. Wallstrom, A. Lobell, T. Olsson, and F. Piehl
Vra4 Congenic Rats with Allelic Differences in the Class II Transactivator Gene Display Altered Susceptibility to Experimental Autoimmune Encephalomyelitis
J. Immunol., March 1, 2008; 180(5): 3289 - 3296.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.