title: The influence of innate immunity gene receptors polymorphisms in renal transplant infections.
abstract: BACKGROUND
  Genetically defined deficiencies in key components of the innate immune system have been associated with a greater risk of infection. The aim of this study was to assess the influence of genetic variability of innate immune receptors (mannose-binding lectin [MBL], mannose-associated serine-protease-2 [MASP-2], and Toll-like receptors [TLR4]) in the risk of infections after a kidney transplantation.
  
  
  METHODS
  All patients undergoing a kidney or kidney-pancreas transplantation during a 3-year period were included. Functionally relevant mutations in MBL2, MASP2, and TLR4 genes were determined by DNA sequencing. The incidence of major bacterial infections, asymptomatic cytomegalovirus (CMV) infection, and CMV disease were compared among groups.
  
  
  RESULTS
  There were no differences regarding major transplant characteristics among groups. Older age, requirements for posttransplant hemodialysis, and pretransplant diabetes, but not gene polymorphisms, were associated with a greater number of bacterial infections. In univariate analysis, low-MBL genotypes were associated with CMV disease in pretransplant CMV seropositive patients (P=0.015), whereas the TLR4 mutation was associated with higher risk of CMV primary infection (P=0.024). TLR4 mutation was an independent factor associated with CMV disease (odds ratio 5.84, 95% confidence interval 1.35-25.20, P=0.018).
  
  
  CONCLUSIONS
  Polymorphisms of innate immunity receptors, especially TLR4 mutation, were associated with higher risk of CMV disease, while susceptibility to other infectious disorders was not observed.
authors.affiliation: Department of Infectious Diseases, Hospital Clínic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Faculty of Medicine, University of Barcelona, Barcelona, Spain.
authors.forename: Carlos
authors.initials: C
authors.lastname: Cervera
authors.forename: Francisco
authors.initials: F
authors.lastname: Lozano
authors.forename: Nuria
authors.initials: N
authors.lastname: Saval
authors.forename: Idoia
authors.initials: I
authors.lastname: Gimferrer
authors.forename: Ana
authors.initials: A
authors.lastname: Ibañez
authors.forename: Belen
authors.initials: B
authors.lastname: Suárez
authors.forename: Laura
authors.initials: L
authors.lastname: Linares
authors.forename: Federico
authors.initials: F
authors.lastname: Cofán
authors.forename: Maria Jose
authors.initials: MJ
authors.lastname: Ricart
authors.forename: Nuria
authors.initials: N
authors.lastname: Esforzado
authors.forename: María Angeles
authors.initials: MA
authors.lastname: Marcos
authors.forename: Tomás
authors.initials: T
authors.lastname: Pumarola
authors.forename: Federico
authors.initials: F
authors.lastname: Oppenheimer
authors.forename: Josep M
authors.initials: JM
authors.lastname: Campistol
authors.forename: Asunción
authors.initials: A
authors.lastname: Moreno
mesh_terms: D001424:Bacterial Infections / Q000209:etiology* / Q000235:genetics; D003586:Cytomegalovirus Infections / Q000209:etiology* / Q000235:genetics; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics*; D016030:Kidney Transplantation / Q000009:adverse effects*; D037601:Mannose-Binding Lectin / Q000235:genetics*; D009154:Mutation; D011110:Polymorphism, Genetic; D051197:Toll-Like Receptor 4 / Q000235:genetics*
chemical_list: D037601:Mannose-Binding Lectin; C495345:TLR4 protein, human; D051197:Toll-Like Receptor 4