Analysis of TNF-β, IL-10, and IL-1 Cluster Gene Polymorphisms and Clinical Risk Factors on Acute Renal Graft Rejection

Acute rejection (AR) still represents a major clinical problem accounting for most renal graft failures and hinders the success of renal transplantation. There is growing evidence of the genetic association between certain cytokine or its receptor antagonist and AR after renal transplantation. Some studies [1-3] investigated the association of IL1β, IL-1 receptor antagonist (IL-1ra) or TNF-β gene polymorphism with acute renal graft rejection. However, the effects of these polymorphisms on AR after renal transplantation are still controversial. Panel reactive antibodies (PRA) are pre-existing antibodies targeting the human leukocyte antigen (HLA) and the complement system has an essential role in PRA related kidney rejection by the classical C1q-dependent pathway [4]. Although it has been established that elevated PRA can induce severe AR in renal transplantation [5,6], pre-transplant PRA levels were only involved in limited studies [7-11] which investigated the association of gene polymorphism with acute renal graft rejection. We sought to ascertain whether polymorphisms of the genes encoding recipients TNF β, IL-10 and IL-1β and IL-1ra as well as other variables such as PRA levels and HLA mismatches had impacts on the incidence of acute renal graft rejection and among these variables, which the most important risk factor for AR was.