title: Disease phenotypes and gender association of FCRL3 single-nucleotide polymorphism -169T/C in Taiwanese patients with systemic lupus erythematosus and rheumatoid arthritis.
abstract: OBJECTIVE
  To investigate the association of the functional FCRL3 single-nucleotide polymorphism (SNP) -169T/C with disease phenotypes and susceptibility to systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) in Taiwanese.
  
  
  METHODS
  FCRL3 SNP -169T/C was genotyped in 573 patients with SLE, 670 patients with RA, and 758 controls. Genotype distributions and allele frequencies were compared among the 3 groups as aggregates or as stratified by clinical characteristics, autoantibody profile, and sex within patient groups.
  
  
  RESULTS
  Overall, FCRL3 SNP -169T/C was not associated with susceptibility to either SLE or RA. However, -169CC genotype was significantly reduced in leukopenia-positive SLE patients as compared to the leukopenia-negative SLE patients (CC vs CT+TT, p = 6 × 10(-4), OR 0.444, 95% CI 0.279-0.708) and controls (p = 6.1 × 10(-3), OR 0.583, 95% CI 0.396-0.857). On the other hand, -169TT genotypes were significantly more numerous in RA patients with non-destructive disease as compared with patients with destructive disease (CC+CT vs TT: p = 0.007, OR 1.672, 95% CI 1.149-2.432). The -169T allele frequency was also significantly increased in non-destructive RA compared with patients with destructive disease (C vs T: p = 0.010, OR 1.423, 95% CI 1.089-1.859). FCRL3 SNP -169TT homozygous donors were significantly more numerous among female cyclic citrullinated peptide (CCP)-negative RA patients versus female CCP-positive RA patients (CC+CT vs TT: p = 0.019, OR 1.64, 95% CI 1.085-2.479).
  
  
  CONCLUSIONS
  The functional FCRL3 SNP -169T/C appears to play important roles in the development of certain phenotypes such as SLE leukopenia and RA disease severity in Taiwanese patients with SLE and RA.
authors.affiliation: Department of Medicine, Division of Clinical Immunology and Rheumatology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
authors.forename: Ji-Yih
authors.initials: JY
authors.lastname: Chen
authors.forename: Chin-Man
authors.initials: CM
authors.lastname: Wang
authors.forename: Yeong-Jian Jan
authors.initials: YJ
authors.lastname: Wu
authors.forename: Shin-Ning
authors.initials: SN
authors.lastname: Kuo
authors.forename: Chiung-Fang
authors.initials: CF
authors.lastname: Shiu
authors.forename: Su-Wei
authors.initials: SW
authors.lastname: Chang
authors.forename: Yen-Tsun
authors.initials: YT
authors.lastname: Lin
authors.forename: Huei-Huang
authors.initials: HH
authors.lastname: Ho
authors.forename: Jianming
authors.initials: J
authors.lastname: Wu
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000483:Alleles; D001172:Arthritis, Rheumatoid / Q000235:genetics*; D001323:Autoantibodies; D002648:Child; D005260:Female; D005787:Gene Frequency; D056726:Genetic Association Studies; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D016015:Logistic Models; D008180:Lupus Erythematosus, Systemic / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D020641:Polymorphism, Single Nucleotide; D011971:Receptors, Immunologic / Q000235:genetics*; D012720:Severity of Illness Index; D011795:Surveys and Questionnaires
chemical_list: D001323:Autoantibodies; C457775:FCRL3 protein, human; D011971:Receptors, Immunologic