Abstract

The development of molecular biological techniques during the last decade has led to the recognition of a series of polymorphic sites in the regulatory regions of cytokine-encoding genes. Different alleles are associated with the binding of transcriptional factors and various degrees of cytokine production [42,110,123]. Therefore each person has an individual profile of high and low cytokine responses. Some individuals are more susceptible to inflammatory conditions [110] and the development of an immune response after transplantation [62]. It has been documented that in heart transplantation high TNF-α/low IL-10 producers had high levels of graft rejection [121], while in renal transplants high TNF- α /high IL-10 producers were characterized with worse prognosis [106]. The polymorphic features of genes encoding cytokines also associate with the outcome of bone marrow transplantation [28]. It was shown that recipient TNFd, IFN- γ (CA) and IL-10[sup]–1064[/sup] microsatellite polymorphisms [19,20] and IL-10 (–1082) and IL-6 (–174) SNP polymorphisms are associated with acute GvHD manifestation [19,68,109]. No relation was found between TNFA (–308) and aGvHD [15]. Recently, the influence of donor polymorphism within the IL-10 and IL-6 genes was documented [68,109]. Polymorphism of the TNFd, TNFA (–308), TNFA (–238), TNFB (–252), and IFN- γ (+874) genes in donors were not related to this complication [131]. In addition, donor and recipient IL-6 gene polymorphism and recipient IFN- γ and IL-10 alleles were described as risk factors of cGvHD [109,131].

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