Analysis of CC chemokine receptor 5 and 2 polymorphisms and renal transplant survival

Yigit B., Bozkurt N., Berber İ., Titiz I., Isbir T.

CELL BIOCHEMISTRY AND FUNCTION, vol.25, no.4, pp.423-426, 2007 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 25 Issue: 4
  • Publication Date: 2007
  • Doi Number: 10.1002/cbf.1322
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.423-426
  • Keywords: acute renal rejection, CCR2 receptor, CCR5 receptor, polymorphism, ACUTE REJECTION, EXPRESSION, PROMOTER
  • Acibadem Mehmet Ali Aydinlar University Affiliated: No


Chronic rejection is an immune process leading to graft failure. By regulating the trafficking of leukocytes, chemokines and chemokine receptors are thought to be one of the reasons causing acute renal rejection (ARE), which increases the possibility of chronic rejection and organ destruction. This study was designed to investigate, in the Turkish population, an association of chemokine receptor genetic variants, CCR2V641, CCR5-59029-A/G, CCR5-A32 and acute renal rejection after renal transplant surgery. We carried out our study in 85 Turkish renal transplant patients (45 men, 40 women; mean age 39 2 years) by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) techniques. We found no significant difference in the incidence of rejection among patients possessing or lacking CCR5-A32. For the groups with and without acute renal rejection, we found a significant difference between the groups in A and G allele distribution in both CCR2V641 and CCR559029 gene variants (p = 0.003 and p = 0.003, respectively). According to our findings, the risk of acute rejection in renal transplantation may be associated with genetic variation in the chemokine receptor genes CCR559029 and CCR2V641 in Turkey, and studies on these gene polymorphisms could be an ideal target for future interventions intended to prevent renal transplant loss. Copyright (C) 2006 John Wiley & Sons, Ltd.