Clinical impact of cytokine gene polymorphisms in heart and lung transplantation

Abstract

During the past decades, the success of heart and lung transplantations increased largely because of the introduction of new, more effective, and more specific immunosuppressive drugs. However, complications resulting in severe morbidity and mortality remain. These complications include acute rejection; chronic rejection, manifesting as transplant coronary artery disease (TCAD) or bronchiolitis obliterans syndrome (BOS); renal failure; post-transplant lymphoproliferative disorder; and infections. All these problems originate from a combination of allogen-dependent and -independent factors in the context of recipient and donor variabilities under circumstances of immunosuppression. A number of these factors are controlled genetically by variations in genome sequences, polymorphisms that consequently may influence the development and progression of transplant-related problems. Of the more than 2 million known polymorphisms in the human genome, specific attention in transplant medicine has been paid to variations in the genes that encode cytokines. These soluble mediators are assumed to play a critical role in the pathogenesis of complications observed after organ transplantation.