ABSTRACT
Ischemia reperfusion damage usually occurs after renal transplantation. These injuries can stimulate the innate immune system, trigger an inflammatory response and ultimately activate the adaptive immune system. These events may result in rejection, graft fibrosis and chronicallograft nephropathy. Different mechanisms contribute to innate immune system activation following ischemia reperfusion injury in renal transplants. Some of these mechanisms are known and described by investigators while the remaining are still unknown. To clarify the precise mechanisms underlying the innate immune system activation and rejection progression helps us to plan therapeutic protocols to reduce immunologic responses to ischemic events and to improve the graft function and outcome. In this review, we will discuss how innate and adaptive immune systems are activated during an ischemic insult and thereafter discuss related therapeutic interventions to block the activating pathways
ABSTRACT
Despite advances in the medical care of renal transplant recipients which have led to an improvement in allograft survival, renal allograft rejection is still a major obstacle to successful organ transplantation. Understanding the mechanisms contributing to allograft rejection will be of great importance for the development of efficient antirejection strategies. The aim of current investigation was to study the impact of polymorphisms of CCR5 delta 32, CCR5- 59029 A/G and CCR2-V64I on renal allograft survival. Using PCR and PCR-RFLP methods in 84 renal transplant recipients, the influence of CCR5 delta 32, CCR5- 59029 A/G and CCR2-V64I polymorphisms on renal allograft survival in two rejector and non-rejector groups were examined. Rejector group was defined as having rejection before 1 year and non-rejector group had stable graft function at least for 5 years. Significant reductions were found in the risk of renal transplant rejection in recipients possessing the CCR2-64I [A] allele [p=0.03] or 59029-A allele [p=0.03] compared to non-rejector group. There were no significant differences in the frequency of CCR5 DELTA 32 polymorphism in rejector group compared to non-rejector group [p>0.05]. It was possible to conclude that the chemokine receptors CCR2-V64I [A] and CCR5- 59029 A alleles may influence renal allograft survival