title: CD86 +1057G>A polymorphism and susceptibility to acute kidney allograft rejection.
abstract: BACKGROUND
  CD86 is a costimulatory molecule that participates in the regulation of T-cell lymphocytes activation. Thus, we examined a genetic marker on the CD86 gene in kidney transplant outcome.
  
  
  METHODS
  In our retrospective study, 168 kidney allograft recipients were genotyped by direct sequencing. Patients were classified into 2 groups of 29 human leukocyte antigen (HLA)-identical haplotype allograft recipients and 139 recipients showing one or more mismatches in the HLA haplotype. Forty-five patients (26.8%) developed at least 1 acute rejection (AR) episode, 7 in the first and 38 in the second group.
  
  
  RESULTS
  Acute rejection was associated with the presence anti-HLA antibodies before transplantation (P = .03). The AA genotype and A allele at position +1057 in the CD86 gene were more frequent in patients without AR (9.75% and 28.5%, respectively) compared with those showing an AR (2.22% and 23.3%, respectively). This difference was statistically significant in the anti-HLA-positive recipients, as AA frequency was 31.3% in non-AR patients and zero in AR ones (P = .04) and A allele frequency was 46.9% and 20.8%, respectively (P = .04). Patients bearing AA genotype reached a higher graft survival time (9.84 years) than those carrying GA (8.21 years, P = .32) or GG (7.61 years, P = .72) genotypes.
  
  
  CONCLUSIONS
  These results suggest that AA genotype and A allele of CD86 +1057G>A polymorphism may confer a protection against acute kidney allograft rejection in Tunisian patients.
authors.affiliation: Immunology Research Laboratory of Kidney Transplantation and Immunopathology, University Tunis El Manar, Charles Nicolle Hospital, Tunis, Tunisia.
authors.forename: Henda
authors.initials: H
authors.lastname: Krichen
authors.forename: Imen
authors.initials: I
authors.lastname: Sfar
authors.forename: Rafika
authors.initials: R
authors.lastname: Bardi
authors.forename: Taieb
authors.initials: T
authors.lastname: Ben Abdallah
authors.forename: Salwa
authors.initials: S
authors.lastname: Jendoubi-Ayed
authors.forename: Walid
authors.initials: W
authors.lastname: Ben Aleya
authors.forename: Mouna
authors.initials: M
authors.lastname: Makhlouf
authors.forename: Thouraya
authors.initials: T
authors.lastname: Ben Rhomdhane
authors.forename: Houda
authors.initials: H
authors.lastname: Aouadi
authors.forename: Ezzeddine
authors.initials: E
authors.lastname: Abderrahim
authors.forename: Khaled
authors.initials: K
authors.lastname: Ayed
authors.forename: Yousr
authors.initials: Y
authors.lastname: Gorgi
mesh_terms: D000208:Acute Disease; D000328:Adult; D051940:B7-2 Antigen / Q000235:genetics* / Q000276:immunology; D004247:DNA / Q000235:genetics*; D005260:Female; D005500:Follow-Up Studies; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006084:Graft Rejection / Q000453:epidemiology / Q000235:genetics* / Q000276:immunology; D006801:Humans; D007111:Immunity, Cellular / Q000235:genetics*; D015994:Incidence; D007676:Kidney Failure, Chronic / Q000601:surgery; D016030:Kidney Transplantation; D008213:Lymphocyte Activation / Q000235:genetics; D008297:Male; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012189:Retrospective Studies; D013601:T-Lymphocytes / Q000276:immunology; D013997:Time Factors; D014184:Transplantation, Homologous; D014416:Tunisia / Q000453:epidemiology
chemical_list: D051940:B7-2 Antigen; D004247:DNA