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Rheumatology Advance Access originally published online on June 27, 2007
Rheumatology 2007 46(9):1417-1421; doi:10.1093/rheumatology/kem167
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© The Author 2007. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Association between SLE nephritis and polymorphic variants of the CRP and Fc{gamma}RIIIa genes

A. Jönsen, I. Gunnarsson1, B. Gullstrand2, E. Svenungsson1, A. A. Bengtsson, O. Nived, I. E. Lundberg1, L. Truedsson2 and G. Sturfelt

Department of Clinical Sciences, Section of Rheumatology, Lund University Hospital, SE-221 85, 1Rheumatology Unit, Department of Medicine, Karolinska University Hospital, Solna, Karolinska Institutet, SE-171 76, Stockholm, Sweden and 2Department of Laboratory Medicine, Section of Microbiology, Immunology and Glycobiology, Lund University, Sölvegatan 23, SE-223 62, Lund

Correspondence to: A. Jönsen, Department of Rheumatology, Lund University Hospital, S-22185 Lund, Sweden. E-mail: Andreas.Jonsen{at}med.lu.se


  Abstract

Objectives. To study the relationship between clinical manifestations in systemic lupus erythematosus (SLE) with polymorphisms in suggested susceptibility genes encoding Fc{gamma}RIIa, Fc{gamma}RIIIa, Fc{gamma}RIIIb, CRP and IL-1Ra.

Methods. Genetic polymorphisms were analysed in 323 unrelated SLE patients and 200 healthy blood donors. The genotype frequencies were compared between clinical subsets of SLE patients, as well as with healthy controls. Clinical manifestations included the ACR classification criteria. Nephritis was further classified according to WHO class on renal biopsy.

Results. Presence of a CRP4 A-allele was associated with SLE nephritis (P < 0.01) and inversely correlated with arthritis (P < 0.01), when comparing within the SLE group. The Fc{gamma}RIIIa F/F genotype was also associated with nephritis (WHO class III and IV, P = 0.04 for the SLE group) and in combination with the CRP4 A-allele a stronger association was noted (P < 0.001). Furthermore, the Fc{gamma}RIIIb NA2/NA2 genotype was associated with butterfly rash (P < 0.01). An association was found between seizures and the presence of both the Fc{gamma}RIIa R/R and the Fc{gamma}RIIIa F/F genotypes (P < 0.01) and an inverse correlation between serositis and the CRP4 A-allele when present together with the IL-1Ra 2-allele (P = 0.01). Furthermore, a combination of the Fc{gamma}RIIa R/R genotype and CRP4 A-allele was associated with lymphopenia (P = 0.02) and a similar result was found for the combination of Fc{gamma}RIIIa F/F and Fc{gamma}RIIIb NA2/NA2 (P = 0.04).

Conclusions. Polymorphic variants of the CRP and Fc{gamma}-receptor genes are associated with the clinical phenotype in SLE. Our findings suggest an immune complex-mediated pathogenesis in nephritis and seizures, while development of arthritis may depend on other pathogenetic pathways.

KEY WORDS: Systemic lupus erythematosus, C-reactive protein, Fc receptor, Genetic, Polymorphism, Glomerulonephritis

Submitted 31 January 2007; revised version accepted 18 May 2007.
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