ab2005

CC chemokine receptor 5 and interleukin-1 receptor antagonist gene polymorphisms in patients with primary Sjögren's syndrome

M. Petrek¹, Z. Cermáková^1*, B. Hutyrová^1*, D. Miceková², J. Drábek¹, J. Rovensky², V. Bosák²

¹Department of Immunology, Palacky University, Olomouc, Czech Republic; ²Research Institute of Rheumatic Diseases, Piest'any, Slovak Republic.

ABSTRACT
Objective
Interleukin-1 receptor antagonist (IL-1Ra) and also mononuclear cell-attractant chemokines CCL3, CCL4 and CCL5 have been implicated in the immunopathogenesis of primary Sjögren syndrome (pSS). Both the gene coding for receptor CCR5 binding the aforementioned CCL ligands and the gene for IL-1Ra are polymorphic. We have therefore in a case control study assessed the putative role of these "candidate" polymorphic genes in the inflammatory process in Sjšgren syndrome.

Methods
DNA was obtained from 39 unrelated patients with primary Sjögren.s syndrome and 76 unrelated healthy controls; all subjects were Caucasians of Slovak origin. CCR5D32 and IL-1Ra VNTR polymorphisms were genotyped by PCR-SSP.
Results. The frequencies of CCR5D32 in patients with pSS were different from that in control subjects: there was an apparent decrease of the mutant allele in the patient group. CCR5D32/CCR5 heterozygosity was associated with a reduced relative risk of pSS (OR 0.35, p = 0.043). There was no difference in the distribution of the alleles of the IL-1Ra VNTR polymorphism between the groups of pSS patients and control subjects.

Conclusion
In this population of patients with Sjögren's syndrome, the frequency of CCR5D32/CCR5 genotype is significantly decreased. The data suggests that carrier status for the CCR5 D32 allele may contribute to protection from the development of primary Sjögren's syndrome. In contrast, IL-1Ra VNTR polymorphism does not confer susceptibility to primary Sjögren's syndrome in Slovak Caucasians.

Key words
CCR5, D32 allele, IL-1 receptor antagonist, VNTR, polymorphism, Sjögren's syndrome.

*The authors Z. Cermáková and B. Hutyrová equally contributed to this work.
This work was supported by the Grant Agency of the Czech Republic (GACR 310/99/1676) and partially also by Czech governmental funding (MSM15100002).
Part of this work was presented at the 10th Meeting of the Czech and Slovak Immunological Societies, Liberec 25-28th October 2000.
Please address correspondence to: Dr. Martin Petrek, Department of Immunology, Tissue Typing Laboratory, Medical Faculty of Palacky University, I.P. Pavlova no. 6, 775 20 Olomouc, Czech Republic.
E-mail: petrekm@fnol.cz