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Rheumatology International
Published in: Rheumatology International 2/2016

01-02-2016 | Original Article - Genes and Disease

MHC2TA and FCRL3 genes are not associated with rheumatoid arthritis in Mexican patients

Authors: J. F. Mendoza Rincón, A. K. Rodríguez Elias, J. M. Fragoso, G. Vargas Alarcón, K. Maldonado Murillo, M. L. Rivas Jiménez, R. E. Barbosa Cobos, S. Jimenez Morales, G. Lugo Zamudio, C. Tovilla Zárate, J. Ramírez Bello

Published in: Rheumatology International | Issue 2/2016

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Abstract

Rheumatoid arthritis (RA) is a multifactorial disease. A combination of genetic and environmental risk factors contributes to its etiology. Several genes have been reported to be associated with susceptibility to the development of RA. The MHC2TA and FCRL3 genes have been associated previously with RA in Swedish and Japanese populations, respectively. In two recent reports, we show an association between FCRL3 and juvenile rheumatoid arthritis (JRA), and MHC2TA and acute coronary syndrome (ACS) in Mexican population. We assessed the association between three single nucleotide polymorphisms (SNPs) of the MHC2TA (−168G/A; rs3087456, and +16G/C; rs4774) and FCRL3 (−169T/C; rs7528684) genes and rheumatoid arthritis in Mexican population through a genotyping method using allelic discrimination assays with TaqMan probes. Our case–control study included 249 patients with RA and 314 controls. We found no evidence of an association between the MHC2TA −168G/A and +1614G/C or FCRL3 −169T/C polymorphisms and RA in this Mexican population. In this cohort of Mexican patients with RA, we observed no association between the MHC2TA or FCRL3 genes and this autoimmune disease.
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Metadata
Title
MHC2TA and FCRL3 genes are not associated with rheumatoid arthritis in Mexican patients
Authors
J. F. Mendoza Rincón
A. K. Rodríguez Elias
J. M. Fragoso
G. Vargas Alarcón
K. Maldonado Murillo
M. L. Rivas Jiménez
R. E. Barbosa Cobos
S. Jimenez Morales
G. Lugo Zamudio
C. Tovilla Zárate
J. Ramírez Bello
Publication date
01-02-2016
Publisher
Springer Berlin Heidelberg
Published in
Rheumatology International / Issue 2/2016
Print ISSN: 0172-8172
Electronic ISSN: 1437-160X
DOI
https://doi.org/10.1007/s00296-015-3358-2

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