Chemokine receptor 5Delta32 mutation reduces the risk of acute rejection in liver transplantation
- PMID: 19644158
Chemokine receptor 5Delta32 mutation reduces the risk of acute rejection in liver transplantation
Abstract
Background: Chemokine receptor 5 (CCR-5) plays a central role in allograft rejection. CCR-5Delta32 mutation results in a non-functioning receptor. Homozygous CCR-5Delta32 patients show a significantly improved kidney graft survival rate compared to CCR-5 wild-type patients. Similar correlations between the CCR-5Delta32 genotype and acute rejection or graft survival rate were shown for heart, lung and islet cell transplantation.
Material/methods: The aim of this study was to examine CCR-5Delta32 and acute rejection after liver transplantation (OLT). 158 OLT patients were genotyped. Data of grafts and patients were collected prospectively into a transplant database.
Results: There were no significant differences between groups regarding patient, donor or graft variables. CCR-5 wild-type patients had explicitly more acute rejection episodes (p=0.086) than patients with the heterozygous or homozygous Delta32-mutation. Homozygous Delta32 patients had no acute rejection episodes. 12.5% of heterozygous patients had one acute rejection episode as opposed to 30.6% of wild-type patients. Only wild-type patients experienced more than one rejection episode.
Conclusions: Patients with the Delta32-mutation might be candidates for a minimized immunosuppressive therapy. CCR-5 could be relevant as a target for a new therapeutic approach.
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