Normothermic Ischemia Induces Major Histocompatibility Complex Class I Expression in Hepatocytes

Gugenheim, Jean; Reynès, M; Crafa, Francesco; Saint–Paul, Marie–Christine; Fabiani, B; Mouïel, J

doi:10.1159/000129464

Cited by 3 publications

(2 citation statements)

References 13 publications

(17 reference statements)

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“…In a previous study, we showed that severe IRI to hepatocytes, as reflected by a high peak alanine aminotransferase, was also an important risk factor for NAS development . Interestingly, Gugenheim et al demonstrated an upregulation of hepatic class I antigen expression after a period of normothermic ischemia in a rat model …”

Section: Discussionmentioning

confidence: 99%

“…10 Interestingly, Gugenheim et al demonstrated an upregulation of hepatic class I antigen expression after a period of normothermic ischemia in a rat model. 37 It could therefore be expected that a relation exists between IRI, the presence of antibodies against donor HLA antigens expressed on hepatocytes and biliary epithelium and bile duct complications, DSA are related to an inferior clinical outcome after OLT. 7,9 Sensitivity analysis was performed in the current study for MFI>1000 with similar outcomes.…”

Section: Discussionmentioning

confidence: 99%

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Donor‐specific anti‐HLA antibodies are not associated with nonanastomotic biliary strictures but both are independent risk factors for graft loss after liver transplantation

Dulk

Shi

Verhoeven

et al. 2017

Clinical Transplantation

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Donor-specific alloantibodies (DSA) have been associated with rejection and shorter graft survival after orthotopic liver transplantation (OLT). We examined the role of DSA in nonanastomotic biliary strictures (NAS) after OLT. Patients receiving first OLT who developed NAS (n = 68) and a control group without NAS (n = 83), with pre-OLT and 12 months post-OLT serum samples, were included. DSA were specified using the Luminex single antigen test. Risk factors for NAS and graft survival were analyzed. The presence of preformed DSA was not significantly different between patients with NAS and controls (P = .89). After 12 months, 26.5% of NAS patients and 16.9% of controls had generated de novo DSA (P = .15). Neither de novo class I DSA nor de novo class II DSA were associated with NAS. De novo DSA generally developed after the diagnosis of NAS. Time-dependent regression analysis identified both NAS (aHR 8.05, CI 3.28 -19.77, P < .01) and de novo class II DSA (aHR 2.84, CI 1.38 -5.82, P < .01) as independent risk factors for graft loss. Preformed or de novo DSA were not associated with the development of NAS. However, NAS as well as de novo class II DSA were independent risk factors for graft loss after OLT. K E Y W O R D Sbiliary strictures, complications, donor-specific antibodies, HLA-antibody post-transplantation, liver transplantation, outcomeThis is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Donor‐specific anti‐HLA antibodies are not associated with nonanastomotic biliary strictures but both are independent risk factors for graft loss after liver transplantation

Dulk

Shi

Verhoeven

et al. 2017

Clinical Transplantation

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The Impact of Ischemia/Reperfusion Injury on Specific and Non-Specific, Early and Late Chronic Events After Organ Transplantation

Land

Meßmer

Events

1996

Transplantation Reviews

163

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Protection of Hepatocytes from Cytotoxic T Cell Mediated Killing by Interferon-Alpha

et al. 2007

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BackgroundCellular immunity plays a key role in determining the outcome of hepatitis C virus (HCV) infection, although the majority of infections become persistent. The mechanisms behind persistence are still not clear; however, the primary site of infection, the liver, may be critical. We investigated the ability of CD8+ T-cells (CTL) to recognise and kill hepatocytes under cytokine stimulation.Methods/Principle FindingsResting hepatocytes cell lines expressed low levels of MHC Class I, but remained susceptible to CTL cytotoxicity. IFN-α treatment, in vitro, markedly increased hepatocyte MHC Class I expression, however, reduced sensitivity to CTL cytotoxicity. IFN-α stimulated hepatocyte lines were still able to present antigen and induce IFN-γ expression in interacting CTL. Resistance to killing was not due to the inhibition of the FASL/FAS- pathway, as stimulated hepatocytes were still susceptible to FAS-mediated apoptosis. In vitro stimulation with IFN-α, or the introduction of a subgenomic HCV replicon into the HepG2 line, upregulated the expression of the granzyme-B inhibitor–proteinase inhibitor 9 (PI-9). PI-9 expression was also observed in liver tissue biopsies from patients with chronic HCV infection.Conclusion/SignificanceIFN-α induces resistance in hepatocytes to perforin/granzyme mediate CTL killing pathways. One possible mechanism could be through the expression of the PI-9. Hindrance of CTL cytotoxicity could contribute to the chronicity of hepatic viral infections.

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Normothermic Ischemia Induces Major Histocompatibility Complex Class I Expression in Hepatocytes

Cited by 3 publications

References 13 publications

Donor‐specific anti‐HLA antibodies are not associated with nonanastomotic biliary strictures but both are independent risk factors for graft loss after liver transplantation

Donor‐specific anti‐HLA antibodies are not associated with nonanastomotic biliary strictures but both are independent risk factors for graft loss after liver transplantation

The Impact of Ischemia/Reperfusion Injury on Specific and Non-Specific, Early and Late Chronic Events After Organ Transplantation

Protection of Hepatocytes from Cytotoxic T Cell Mediated Killing by Interferon-Alpha

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