The role of interleukin-10 promoter polymorphisms in primary Sjögren's syndrome

• Published in: Scandinavian journal of rheumatology Vol. 37; no. 4; pp. 293 - 299
• Main Authors: Willeke, P., Gaubitz, M., Schotte, H., Becker, H., Domschke, W., Schlüter, B.
• Format: Journal Article
• Language: English
• Published: Colchester Informa UK Ltd 01.01.2008; Taylor & Francis
• Subjects: Adolescent; Adult; Aged; Aged, 80 and over; Autoantibodies - genetics; Autoantibodies - immunology; Biological and medical sciences; Carrier Proteins - immunology; Case-Control Studies; Diseases of the osteoarticular system; Female; Genetic Predisposition to Disease; Humans; Immunoglobulin A - genetics; Immunoglobulin A - immunology; Interleukin-10 - genetics; Male; Medical sciences; Microfilament Proteins - immunology; Middle Aged; Polymorphism, Single Nucleotide - genetics; Promoter Regions, Genetic; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis; Sjogren's Syndrome - genetics; Promoter; Immunopathology; Eye disease; Stomatology; Systemic disease; Interleukin 10; Rheumatology; Autoimmune disease; Sjögren syndrome; Polymorphism
• ISSN: 0300-9742; 1502-7732
• DOI: 10.1080/03009740801910353

Objective: To determine the impact of a broad spectrum of different polymorphisms within the interleukin-10 (IL-10) promoter gene on disease susceptibility to primary Sjögren's syndrome (pSS), clinical manifestations, and autoantibody production. Methods: We genotyped 111 unrelated German Caucasian patients with pSS and 145 healthy controls for the single nucleotide polymorphisms (SNPs) at positions −2849, −2776, −2769, −2763, −1349, −1082, −851, −819, −657, and −592 and for the microsatellites IL10.R and IL10.G. Allele and haplotype distributions were compared between patients and controls and between subgroups of patients with different clinical and laboratory findings. Results: We found no significant differences in the allele or haplotype frequencies between pSS patients and healthy controls. After Bonferroni correction we found a significant association of the ACC haplotype (at the −1082, −819, and −592 loci) with immunoglobulin (Ig)A antibodies to anti- -fodrin. Conclusion: Overall we found no associations of IL-10 promoter polymorphisms with the susceptibility to pSS in our cohort. The finding that the production of IgA anti- -fodrin antibodies is associated with polymorphisms within the IL-10 promoter region suggests a genetic contribution to the generation of these antibodies.