title: Association of killer cell immunoglobulin-like receptor 2DL5 with systemic lupus erythematosus and accompanying infections.
abstract: OBJECTIVE
  Identification of the association of killer cell immunoglobulin-like receptor (KIR) genes with SLE and accompanying infections.
  
  
  METHODS
  Presence or absence of all 14 KIR genes was studied for association with SLE by case-control studies. A total of 417 SLE cases, 72 RA cases and 256 controls, all of Japanese descent, were enrolled.
  
  
  RESULTS
  The carrier frequency of KIR2DL5 was significantly decreased in SLE patients compared with healthy controls [39.3 vs 50.4%; odds ratio (OR) = 0.64; 95% CI 0.36, 0.92; P = 0.005). When the prevalence of severe infections was analysed in 184 SLE patients, whose medical records were available, KIR2DL5 carriers were at an increased risk of overall infection and viral infection (crude OR = 2.66; 95% CI 1.43, 4.92; P = 0.017 and crude OR = 2.31; 95% CI 1.15, 4.62; P = 0.017, respectively). After adjusting for methylprednisolone pulse and/or cyclophosphamide pulse therapy, KIR2DL5 carriers were at significantly greater risk of infectious events overall (adjusted OR = 2.45; 95% CI 1.24, 4.81; P = 0.0095). However, KIR2DL5 carriers were marginally associated with an increased risk of viral infectious events (adjusted OR = 2.03; 95% CI 0.94, 4.41; P = 0.0718).
  
  
  CONCLUSIONS
  KIR2DL5 was significantly associated with a decreased risk of SLE as well as an increased risk of infectious events overall in SLE patients. Our data suggest a further role of KIRs in the pathogenesis of autoimmune diseases and infection.
authors.affiliation: Department of Medicine and Biosystemic Science, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.
authors.forename: Yasutaka
authors.initials: Y
authors.lastname: Kimoto
authors.forename: Takahiko
authors.initials: T
authors.lastname: Horiuchi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Tsukamoto
authors.forename: Chikako
authors.initials: C
authors.lastname: Kiyohara
authors.forename: Hiroki
authors.initials: H
authors.lastname: Mitoma
authors.forename: Ayumi
authors.initials: A
authors.lastname: Uchino
authors.forename: Isao
authors.initials: I
authors.lastname: Furugo
authors.forename: Seiji
authors.initials: S
authors.lastname: Yoshizawa
authors.forename: Akira
authors.initials: A
authors.lastname: Ueda
authors.forename: Shinichi
authors.initials: S
authors.lastname: Harashima
authors.forename: Takuya
authors.initials: T
authors.lastname: Sawabe
authors.forename: Tomoko
authors.initials: T
authors.lastname: Tahira
authors.forename: Kenshi
authors.initials: K
authors.lastname: Hayashi
authors.forename: Shigeru
authors.initials: S
authors.lastname: Yoshizawa
authors.forename: Terufumi
authors.initials: T
authors.lastname: Shimoda
authors.forename: Koichi
authors.initials: K
authors.lastname: Akashi
authors.forename: Mine
authors.initials: M
authors.lastname: Harada
mesh_terms: D044466:Asian People / Q000235:genetics; D016022:Case-Control Studies; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000235:genetics* / Q000276:immunology; D011110:Polymorphism, Genetic; D054346:Receptors, KIR2DL5 / Q000235:genetics* / Q000276:immunology; D012044:Regression Analysis
chemical_list: D054346:Receptors, KIR2DL5