MHC2TA and FCRL3 genes are not associated with rheumatoid arthritis in Mexican patients.
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.
Laboratorio de Oncología Molecular, Unidad de Diferenciación Celular y Cáncer, FES-Zaragoza, UNAM, Mexico City, Mexico.
J F
JF
Mendoza Rincón
Programa de Maestría en Biología Experimental, UAM-I, México City, Mexico.|Laboratorio de Medicina Genómica, Unidad de Investigación, Hospital Juárez de México, Av. Instituto Politécnico Nacional No. 5160, Delegación Gustavo A. Madero, C.P. 07760, Mexico City, D.F, Mexico.
A K
AK
Rodríguez Elias
Departamento de Biología Molecular, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.
J M
JM
Fragoso
Departamento de Biología Molecular, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.
G
G
Vargas Alarcón
Licenciatura en Biología, Facultad de Estudios Superiores, Zaragoza, UNAM, Mexico City, Mexico.
K
K
Maldonado Murillo
Servicio de Reumatología, Hospital Lic. Adolfo López Mateos, Mexico City, Mexico.
M L
ML
Rivas Jiménez
Servicio de Reumatología, Hospital Juárez de México, Mexico City, Mexico.
R E
RE
Barbosa Cobos
Dirección de Investigación, Instituto Nacional de Medicina Genómica, Mexico City, Mexico.
S
S
Jimenez Morales
División de Medicina, Hospital Juárez de México, Mexico City, Mexico.
G
G
Lugo Zamudio
División Académica Multidisciplinaria de Comalcalco, Universidad Juárez Autónoma de Tabasco, Comalcalco, Tabasco, Mexico.
C
C
Tovilla Zárate
Laboratorio de Medicina Genómica, Unidad de Investigación, Hospital Juárez de México, Av. Instituto Politécnico Nacional No. 5160, Delegación Gustavo A. Madero, C.P. 07760, Mexico City, D.F, Mexico. dr.julian.ramirez.hjm@gmail.com.
J
http://orcid.org/0000-0002-4153-9315
J
Ramírez Bello
D000328:Adult; D001172:Arthritis, Rheumatoid / Q000175:diagnosis / Q000453:epidemiology / Q000235:genetics*; D016022:Case-Control Studies; D005260:Female; D005787:Gene Frequency; D056726:Genetic Association Studies; D020022:Genetic Predisposition to Disease; D006239:Haplotypes; D006801:Humans; D008297:Male; D008800:Mexico / Q000453:epidemiology; D008875:Middle Aged; D009687:Nuclear Proteins / Q000235:genetics*; D010641:Phenotype; D020641:Polymorphism, Single Nucleotide; D011971:Receptors, Immunologic / Q000235:genetics*; D012307:Risk Factors; D015534:Trans-Activators / Q000235:genetics*
C457775:FCRL3 protein, human; C083728:MHC class II transactivator protein; D009687:Nuclear Proteins; D011971:Receptors, Immunologic; D015534:Trans-Activators
FCRL3; MHC2TA; Polymorphism; Rheumatoid arthritis