The FCRL3 −169T>C polymorphism might be associated with some autoantibody presence in patients with SLE in a Polish population. Issue 2 (March 2014)

• Record Type: Journal Article
• Authors: Piotrowski, Piotr; Lianeri, Margarita; Prokop, Edyta; Wudarski, Mariusz; Olesińska, Marzena; Jagodziński, Paweł P.
• Is Part Of: Modern rheumatology. Volume 24:Issue 2(2014)
• Page Start: 296
• Page End: 299
• Publication Date: 2014-03
• Subjects: Rheumatology -- Periodicals; 616.723005
• DOI: 10.3109/14397595.2013.854066
• Languages: English
• ISSNs: 1439-7595

Abstract

<abstract> <title>Abstract</title> <p> <italic>Objectives.</italic> The <italic>Fcrl3</italic> −169T>C (rs7528684) polymorphism has been shown to be a risk factor of various autoimmune diseases, including systemic lupus erythematosus (SLE); however, these results are inconsistent between distinct ethnicities.</p> <p> <italic>Methods.</italic> Using PCR-RFLP we studied the distribution of the <italic>FCRL3 −169T</italic>><italic>C</italic> polymorphism in SLE patients (<italic>n</italic> = 263) and controls (<italic>n</italic> = 528) in a sample from the Polish population.</p> <p> <italic>Results.</italic> We found no significant differences of <italic>FCRL3</italic> −169T>C genotypes and alleles between patients with SLE and healthy individuals. However, in the dominant model we found a significant association between the <italic>FCRL3 −169T</italic>><italic>C</italic> polymorphism and the presence of anti-Scl-70 antibody (Ab) [OR = 4.747 (95 % CI = 1.639–13.749), <italic>p</italic> = 0.0011, <italic>p</italic><sub>corr</sub> = 0.0198]. Moreover, in the dominant model we observed a significant contribution of <italic>FCRL3 −</italic>169T>C to the presence of either anti-La or anti-Scl-70 Abs [OR = 4.378 (95 % CI = 1.793–10.690, <italic>p</italic> = 0.0003, <italic>p</italic><sub>corr</sub> = 0.0054)].</p> <p> <italic>Conclusions.</italic> Our study demonstrated that the <italic>FCRL3 −</italic>169T>C polymorphism is not a risk factor of SLE in the Polish population, but this polymorphism may contribute to autoantibody production in this disease.</p> </abstract>