title: Allograft renal rejection and chemokine polymorphism.
abstract: Chemokines play a major role in the process by which leukocytes are recruited from the bloodstream into the sites of inflammation. Genes for the chemokine receptors CCR5, CCR2 and MCP-1 are characterized by functional polymorphisms implicated in transplant rejection. To investigate this association, we analyzed polymorphisms of CCR5-∆32, CCR5-59029-A/G, CCR2-V64I and MCP-1 G/A (-2518) in 173 renal transplant recipients and 169 healthy blood donors. The patients were classified in two groups: Group-1 (G-1) included 33 HLA-identical recipients and Group-2 (G-2) included 140 (one or more) mismatched graft recipients. Forty-two patients had developed acute rejection episodes (ARs): seven in G-1 and 35 in G-2. Thirteen G-2 patients developed chronic allograft dysfunction (CAD). The genotypic and allelic frequencies of all polymorphisms studied did not reveal significant differences between patients and controls and among G-1 and G-2 recipients. However, a significant risk of acute renal transplant rejection was found in G-1 patients who possessed the CCR2-64I allele (odds ratio 0.24, 95% confidence inter-val [CI], 0.05-1.06; P = 0.035). There was no significant association of this polymorphism and CAD. In conclusion, the observed association of CCR2-64I with AR should be added to the spectrum of immunogenetic factors known to be involved in allograft renal loss.
authors.affiliation: Research Laboratory of Transplantation Immunopathology (LR03SP01), Charles Nicolle Hospital, Tunis, Tunisia. gorgi.yousr@gmail.com
authors.forename: Y
authors.initials: Y
authors.lastname: Gorgi
authors.forename: I
authors.initials: I
authors.lastname: Sfar
authors.forename: S
authors.initials: S
authors.lastname: Jendoubi-Ayed
authors.forename: M
authors.initials: M
authors.lastname: Makhlouf
authors.forename: T Ben
authors.initials: TB
authors.lastname: Rhomdhane
authors.forename: R
authors.initials: R
authors.lastname: Bardi
authors.forename: H
authors.initials: H
authors.lastname: Aouadi
authors.forename: T Ben
authors.initials: TB
authors.lastname: Abdallah
authors.forename: E
authors.initials: E
authors.lastname: Abderrahim
authors.forename: K
authors.initials: K
authors.lastname: Ayed
mesh_terms: D000208:Acute Disease; D000328:Adult; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000235:genetics; D018925:Chemokines / Q000235:genetics*; D002908:Chronic Disease; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D006084:Graft Rejection / Q000235:genetics* / Q000276:immunology; D006801:Humans; D016030:Kidney Transplantation / Q000276:immunology*; D008297:Male; D016017:Odds Ratio; D010641:Phenotype; D011110:Polymorphism, Genetic; D054390:Receptors, CCR2 / Q000235:genetics; D019713:Receptors, CCR5 / Q000235:genetics; D018570:Risk Assessment; D012307:Risk Factors; D014184:Transplantation, Homologous; D016896:Treatment Outcome; D014416:Tunisia; D055815:Young Adult
chemical_list: C111835:CCL2 protein, human; C515334:CCR2 protein, human; D018932:Chemokine CCL2; D018925:Chemokines; D054390:Receptors, CCR2; D019713:Receptors, CCR5