Published online Aug 28, 2014. doi: 10.3748/wjg.v20.i32.11116
Revised: May 14, 2014
Accepted: June 12, 2014
Published online: August 28, 2014
Processing time: 296 Days and 11 Hours
Infection is the leading cause of complication after liver transplantation, causing morbidity and mortality in the first months after surgery. Allograft rejection is mediated through adaptive immunological responses, and thus immunosuppressive therapy is necessary after transplantation. In this setting, the presence of genetic variants of innate immunity receptors may increase the risk of post-transplant infection, in comparison with patients carrying wild-type alleles. Numerous studies have investigated the role of genetic variants of innate immune receptors and the risk of complication after liver transplantation, but their results are discordant. Toll-like receptors and mannose-binding lectin are arguably the most important studied molecules; however, many other receptors could increase the risk of infection after transplantation. In this article, we review the published studies analyzing the impact of genetic variants in the innate immune system on the development of infectious complications after liver transplantation.
Core tip: After liver transplantation, immunosuppressive therapy is needed to avoid allograft rejection that is mainly mediated through adaptive immunological responses. In the setting, the existence of genetic variants of innate immunity receptors may increase the risk of post-transplant infections in comparison with patients carrying wild-type alleles. This manuscript reviews the published studies analyzing the influence of innate immunity gene variants on the development of post-transplant infections and other complications.