Fc-Gamma Receptor Polymorphisms Predispose Patients to Infectious Complications After Liver Transplantation

Abstract

We investigated the impact of polymorphisms in host innate immunoregulatory genes on the development of infectious complications after liver transplantation (LT). 3%), of which one third was methicillin-resistant Staphylococcus aureus. No differences were observed in the incidence of fungal infections or in cytomegalovirus infections with respect to the three gene polymorphisms. Our findings indicate that FcgR SNPs are predisposing factors for BSI and can predict mortality after LT. This study provides a foundation for further prospective studies on a larger scale.

Genetic and Functional Profiling of CD16-Dependent Natural Killer Activation Identifies Patients at Higher Risk of Cardiac Allograft Vasculopathy

“…Previous studies have reported associations between FCGR polymorphisms and adverse infectious events or accelerated atherosclerosis after organ transplant 27,29,30 ; Various factors participate in the alteration of renal function in HTRs, both before e a a and nd nd a a aft ft fter er e HT HT H .…”

“…Th The infl fl fla am a matory ry s signals s s t tha at re e esu su sult lt lt fr fr f om om th he stim mu ula at a i io i n of a a act t ctiv va ating F Fceceptors (Fc-R) f for C C-reactive protein (CR C P) P serum amyloid P P component (SA S P) and d IgG 21 . In addition, the FCGR3A polymorphisms have been reported to contribute to infection susceptibility [22][23][24] and coronary artery diseases 25,26 and predispose patients to severe complications after organ transplantation [27][28][29][30][31] . In the current study, we investigated whether CD16-dependent NK cell activation profiles and FCGR3A polymorphism may be associated with the development of CAV.…”

Effect of Fc-γ Receptor Polymorphism on Rituximab-Mediated B Cell Depletion in ABO-Incompatible Adult Living Donor Liver Transplantation

“…We have recently demonstrated that the FCGR3A SNP in recipients of LT was greatly associated with the susceptibility to severe posttransplant infections, ie, a significantly higher incidence of BSI was observed in the individuals with FCGR3A [158F/V or F/F] than that in the individuals with FCGR3A [158V/V]. 24 This finding might reflect a fact that the affinity for IgG3, which induces vigorous compliment activation and ADCC, is remarkably higher in FcγRIIIa than that in FcγRIIa, and FCGR3A [158F/F or F/V] has much less affinity than FCGR3A [158V/V]. 9,24 Hence, FCGR3A SNPs likely influence innate components of humoral immunity.…”

“…24 This finding might reflect a fact that the affinity for IgG3, which induces vigorous compliment activation and ADCC, is remarkably higher in FcγRIIIa than that in FcγRIIa, and FCGR3A [158F/F or F/V] has much less affinity than FCGR3A [158V/V]. 9,24 Hence, FCGR3A SNPs likely influence innate components of humoral immunity.…”

Fcγ Receptors in Solid Organ Transplantation

“…In a study of post-operative infection in liver transplant patients, individuals that were dually homozygous for the FcγRIIA-131H/H, polymorphism and the polymorphism in FCGR3A (F/F158 that reduces IgG binding affinity) were susceptible to blood-borne infections and increased mortality. This susceptibility was attributed to a reduced binding and clearance of CRP-opsonised bacteria, resulting in overwhelming infection [90•].…”