| How to prevent and treat the acute allograft rejection and infections secondary to organ transplantation has been shown to be a major tough problem puzzling transplant field. In many transplant centers, about one third of the recipients experience acute allograft rejection events and over one third of them ever suffered from infections and few may die, even they receive similarly matched grafts and adopted the same immunosuppression regimen. Acute rejection means a state of insufficient immunosuppression after organ transplantation, whereas infection after transplantation, especially the recurring infections always result from over-immunosuppression. Reasonable immunosuppression without infection complications should have been a major aim of immunosuppressant individualization.According to the functions of the cytokines they release, CD4+T helper cells, crucial ones in acute rejection proceeding, could be classified into three subsets including Th1,Th2 and Th3 cell groups. T helper l(Th1) cells produce interleukin-2, interferon y, tumor necrosis factor and interleukin-1 preferentially, whereas Th2 cells are prone to synthesize IL-4,IL-10,IL-5,IL-6 and IL-13 (as well as others).A Th3 subset, producing high levels of transforming growth factor β(TGF-β) with varying amounts of IL-4 and IL-10 , was identified also. Functionally, Thl cells participate in cell mediated inflammatory immune reaction, and Th2 cells regulate the production of immunoglobulin and facilitate humoral immune reaction. Th3 cells are associated with an immunosuppressive phenotype in experimental models of oral tolerance and autoimmunity. There is no difference between their phenotypes, so a concept of Thl versus Th2 polarized arose. More and more evidence have indicated that the polarization of Th1/Th2 equilibrium is critical to immune response, and abnormal Th1/Th2 polarization may result in many diseases such as infections andautoimmunity diseases. In transplant immunology, Th1 cytokines tend to induce rejection, whereas Th2 cytokines are likely to induce immunologic tolerance benefiting graft survival. Th1/Th2 equilibrium determines the onset and the severity of rejection as well as the induction and the maintenance of immunologic tolerance, as a result, polarization of the equilibrium to Th2 become the major way to induce immunologic tolerance. As cytokines take part in the regulation of allograft rejection and defensive response, cytokines gene polymorphisms affecting transcription activity or function of cytokines should impact the occurrence of rejection and infection. A large number of common single nucleotide polymorphisms (SNPs) of cytokines have been described. Although the function of many these polymorphisms is unknown, evidence is accumulating that some influence gene function, for example, by altering the amino acid sequence of protein (e.g., IL-4 receptor, IL-4R), or by modifying transcription activity of the gene(e.g., TNF-α IL-6, IL-10). The studies in vivo suggest that some of these polymorphisms may affect the susceptibility of infection, allergy and autoimmunity disease. The reports about cytokine genotype affecting renal transplant outcome come out ceaselessly with different description, the majority of which indicate that cytokine and cytokine receptor gene polymorphisms may impact the rejection events. Further more, there are also some investigations focusing on role of cytokine gene polymorphisms in infection events. The previous investigators always discussed on recipient cytokine gene polymorphisms influencing transplant outcome for the lymphocyte of recipient act as an cardinal role in acute rejection, but the cytokines from allograft may also affect the local microenvironment of acute rejection and it had been reported that the polymorphisms in IL-6-174 correlates with the onset and severity of renal allograft rejection. To define the distribution of cytokines and their receptors gene genotype among allograft recipient and donor, and to identify the role of these polymorp...
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