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Rheumatology 2001; 40: 1009-1012
© 2001 British Society for Rheumatology

Original Papers

Mannose binding lectin and Fc{gamma}RIIa (CD32) polymorphism in Spanish systemic lupus erythematosus patients

J. Villarreal*, D. Crosdale1,*,, W. Ollier1, A. Hajeer1, W. Thomson1, J. Ordi, E. Balada, M. Villardell, L.-S. Teh2 and K. Poulton3

Hospital General Vall d'Hebron, Passieg Vall d'Hebron 119-129, Barcelona, Spain,
1 Arthritis and Rheumatism Campaign Epidemiology Unit, School of Epidemiology and Health Sciences, Medical School, University of Manchester, Oxford Road, Manchester M13 9PT,
2 Department of Rheumatology, Blackburn Royal Infirmary, Bolton Road, Blackburn BB2 3LR and
3 Manchester Institute of Nephrology and Transplantation, Manchester Royal Infirmary, Oxford Road, Manchester M13 9WL, UK

Objective. Mannose binding lectin (MBL) and Fc{gamma}RII (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 Fc{gamma}RIIa polymorphisms; similar results were observed for renal affectation.

KEY WORDS: MBL, Fc{gamma}RIIa, Polymorphism, SLE.

* These authors contributed equally to this work.

Correspondence to: D. J. Crosdale, Clinical Sciences Building, Northern General Hospital, Herries Road, Sheffield S5 7AU, UK.


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