Rheumatology Advance Access originally published online on March 14, 2006
Rheumatology 2006 45(9):1096-1100; doi:10.1093/rheumatology/kel058
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No primary association of MICA polymorphism with systemic lupus erythematosus
1Instituto de Biomedicina, CSIC, 2Servicio Inmunología, Hospital Virgen de las Nieves, 3Servicio de Medicina Interna, Hospital San Cecilio, 4Servicio de Medicina Interna, Hospital Virgen de las Nieves, Granada, 5Servicio de Inmunología, Hospital Virgen del Rocío, 6Servicio de Medicina Interna, Hospital Virgen del Rocío, Sevilla, 7Servicio de Reumatología, Hospital Xeral-Calde, Lugo and 8Servicio de Medicina Interna, Hospital Carlos-Haya, Malaga, Spain.
Correspondence to: M. F. González-Escribano, Servicio de Inmunología, Hospital Universitario Virgen del Rocío, Avda Manuel Siurot s/n, 41013 Sevilla, Spain. E-mail: mariaf.gonzalez.sspa{at}juntadeandalucia.es
Objective. To replicate the described association between MHC class I chain-related A (MICA) gene polymorphism and susceptibility to systemic lupus erythematosus (SLE).
Methods. MICA transmembrane microsatellite polymorphism was genotyped using a polymerase chain reaction (PCR)-based method. Genotyping of HLA-B* and DRB1* was performed using PCR and detection with a reverse sequence-specific oligonucleotide (SSO) probe system. Combined data for these three loci (HLA-B*, DRB1* and MICA) were obtained from a total of 333 patients and 361 healthy controls.
Results. Significant association with B*08 [P<10–7, odds ratio (OR) 3.17, 95% confidence interval (CI) 2.02–5.00], DRB1*0301 (P<10–7, OR 2.07, 95% CI 1.59–2.68) and MICA5.1 (P = 0.01, OR 1.23, 95% CI 1.04–1.46) was observed. The combinations DRB1*0301-MICA5.1-B8 and HLA-DRB1*0301-B*08-positive and MICA5-1-negative were more frequent among SLE patients (11.4 vs 3.3% in healthy controls, P = 3.9 x 10–5, OR 3.76, 95% CI 1.85–7.73, and 6.9 vs 1.7%, P = 0.0007, OR 4.32, 95% CI 1.68–13.10, respectively). Additionally, individuals who were HLA-DRB1*0301-B*08-negative and MICA5-1-positive were less frequent among patients (22.2 vs 31.3% in healthy controls, P = 0.007, OR 0.63, 95% CI 0.44–0.89) and the magnitude of the OR was similar to that obtained in individuals negative for all the three factors (OR 0.69, 95% CI 050–0.94). Further analysis performed to detect independent association strongly suggested that the association between MICA5.1 and SLE is secondary to the linkage disequilibrium of this allele with B*08.
Conclusions. Our results do not support an independent association of MICA gene polymorphism with susceptibility to SLE.
KEY WORDS: MICA, HLA-DRB1, HLA-B, SLE, Susceptibility.
* These authors contributed equally to this work
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