OBJECTIVE: Mannose binding lectin (MBL) and FcgammaRII (CD32) polymorphisms have both been implicated as candidate susceptibility genes in systemic lupus erythematosus (SLE). The aim of this study was to evaluate the relationship of these polymorphisms with SLE. METHODS: We studied a cohort of 125 SLE patients from Barcelona, Spain and 138 geographically matched controls. Sequence-specific primer-polymerase chain reaction (SSP-PCR) amplification was used to determine CD32 and MBL structural polymorphisms. MBL haplotypes were established using sequence-specific oligonucleotide probing techniques. RESULTS: Patients carried the MBL codon 54 mutant allele more frequently than controls [odds ratio (OR) 2.2; 95% confidence interval (CI) 1.2-4.0; P=0.007] and the haplotype HY W52 W54 W57 was found to be significantly lower in cases compared with controls (OR 0.6; 95% CI 0.4-0.9; P=0.016). CONCLUSION: The MBL gene codon 54 mutant allele appears to be a risk factor for SLE, whilst haplotypes encoding for high levels of MBL are protective against the disease. Differences between controls and patients were not significant when considering the FcgammaRIIa polymorphisms; similar results were observed for renal affectation.
OBJECTIVE:Mannose binding lectin (MBL) and FcgammaRII (CD32) polymorphisms have both been implicated as candidate susceptibility genes in systemic lupus erythematosus (SLE). The aim of this study was to evaluate the relationship of these polymorphisms with SLE. METHODS: We studied a cohort of 125 SLEpatients from Barcelona, Spain and 138 geographically matched controls. Sequence-specific primer-polymerase chain reaction (SSP-PCR) amplification was used to determine CD32 and MBL structural polymorphisms. MBL haplotypes were established using sequence-specific oligonucleotide probing techniques. RESULTS:Patients carried the MBL codon 54 mutant allele more frequently than controls [odds ratio (OR) 2.2; 95% confidence interval (CI) 1.2-4.0; P=0.007] and the haplotype HY W52 W54 W57 was found to be significantly lower in cases compared with controls (OR 0.6; 95% CI 0.4-0.9; P=0.016). CONCLUSION: The MBL gene codon 54 mutant allele appears to be a risk factor for SLE, whilst haplotypes encoding for high levels of MBL are protective against the disease. Differences between controls and patients were not significant when considering the FcgammaRIIa polymorphisms; similar results were observed for renal affectation.
Authors: S Saevarsdottir; H Kristjansdottir; G Grondal; T Vikingsdottir; K Steinsson; H Valdimarsson Journal: Ann Rheum Dis Date: 2006-01-26 Impact factor: 19.103
Authors: Masja Straetemans; Selma P Wiertsema; Elisabeth A M Sanders; Ger T Rijkers; Kees Graamans; Bert van der Baan; Gerhard A Zielhuis Journal: J Clin Immunol Date: 2005-01 Impact factor: 8.317
Authors: Haidy E Zidan; Norhan A Sabbah; Hoda A Hagrass; Enas A Tantawy; Eman E El-Shahawy; Ghada S Nageeb; Amal Bakry Abdul-Sattar Journal: Mol Biol Rep Date: 2013-12-24 Impact factor: 2.316
Authors: Odirlei André Monticielo; Tamara Mucenic; Ricardo Machado Xavier; João Carlos Tavares Brenol; José Artur Bogo Chies Journal: Clin Rheumatol Date: 2008-01-24 Impact factor: 2.980
Authors: Elisandra Grangeiro de Carvalho; Shirley Ramos da Rosa Utiyama; Lorete Maria da Silva Kotze; Iara Taborda de Messias Reason Journal: Dig Dis Sci Date: 2007-03-28 Impact factor: 3.199
Authors: M A Seelen; L A Trouw; J W A van der Hoorn; F C Fallaux-van den Houten; T W J Huizinga; M R Daha; A Roos Journal: Clin Exp Immunol Date: 2003-11 Impact factor: 4.330