title: Deletion of LCE3C_LCE3B is associated with rheumatoid arthritis and systemic lupus erythematosus in the Chinese Han population.
abstract: OBJECTIVE
  The deletion of LCE3C_LCE3B confers susceptibility to psoriasis and rheumatoid arthritis (RA) in Caucasians. The aim of this study was to investigate the variant involvement in RA in the Chinese Han population and to further explore its potential role in the susceptibility to systemic lupus erythematosus (SLE).
  
  
  METHODS
  LCE3C_LCE3B-del was genotyped in 898 patients with RA and 681 healthy controls. Two single nucleotide polymorphisms (SNPs, rs4112788 and rs4085613) in strong linkage disequilibrium with LCE3C_LCE3B-del were then genotyped in patients with RA (n=1222), SLE (n=870) and healthy controls (n=1031).
  
  
  RESULTS
  The deletion of LCE3C_LCE3B and SNPs rs4112788 and rs4085613 showed an association with RA (allele analysis: p=7.72×10(-4), OR 1.28, 95% CI 1.11 to 1.47; p=6.39×10(-4), OR 1.23, 95% CI 1.09 to 1.38; and p=5.38×10(-4), OR 1.23, 95% CI 1.10 to 1.39, respectively). The two SNPs were also signiﬁcantly associated with SLE (allele analysis: p=7.68×10(-3), OR 1.19, 95% CI 1.05 to 1.36 and p=5.30×10(-3), OR 1.20, 95% CI 1.06 to 1.37).
  
  
  CONCLUSIONS
  This study provides evidence for an association between LCE3C_LCE3B-del and RA in non-Caucasian populations, and SNPs rs4112788 and rs4085613 tagging LCE3C_LCE3B-del were novel susceptibility factors for SLE.
authors.affiliation: Department of Rheumatology and Immunology, Peking University People’s Hospital, Beijing, China.
authors.forename: Xiaolan
authors.initials: X
authors.lastname: Lu
authors.forename: Jianping
authors.initials: J
authors.lastname: Guo
authors.forename: Xujie
authors.initials: X
authors.lastname: Zhou
authors.forename: Ru
authors.initials: R
authors.lastname: Li
authors.forename: Xia
authors.initials: X
authors.lastname: Liu
authors.forename: Yi
authors.initials: Y
authors.lastname: Zhao
authors.forename: Baoli
authors.initials: B
authors.lastname: Zhu
authors.forename: Xiangyuan
authors.initials: X
authors.lastname: Liu
authors.forename: Jianhua
authors.initials: J
authors.lastname: Xu
authors.forename: Ping
authors.initials: P
authors.lastname: Zhu
authors.forename: Xinyu
authors.initials: X
authors.lastname: Wu
authors.forename: Jing
authors.initials: J
authors.lastname: He
authors.forename: Xu
authors.initials: X
authors.lastname: Liu
authors.forename: Hong
authors.initials: H
authors.lastname: Zhang
authors.forename: Zhanguo
authors.initials: Z
authors.lastname: Li
mesh_terms: D000328:Adult; D000368:Aged; D001172:Arthritis, Rheumatoid / Q000208:ethnology / Q000235:genetics*; D044466:Asian People / Q000235:genetics*; D016022:Case-Control Studies; D002681:China / Q000453:epidemiology; D055233:Cornified Envelope Proline-Rich Proteins / Q000235:genetics*; D005260:Female; D017353:Gene Deletion; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D006801:Humans; D015810:Linkage Disequilibrium; D008180:Lupus Erythematosus, Systemic / Q000208:ethnology / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction / Q000379:methods; D020641:Polymorphism, Single Nucleotide; D055815:Young Adult
chemical_list: D055233:Cornified Envelope Proline-Rich Proteins; C549748:LCE3B protein, human; C524768:LCE3C protein, human