Interactions Between KIR3DS1 and HLA-F Activate Natural Killer Cells to Control HCV Replication in Cell Culture.

Autor:	Lunemann S; Department of Virus Immunology, Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany., Schöbel A; Junior Research Group HCV Replication, Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany., Kah J; I. Department of Medicine, Center for Internal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany., Fittje P; Department of Virus Immunology, Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany., Hölzemer A; Department of Virus Immunology, Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany; I. Department of Medicine, Section Infectious Diseases, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; German Center for Infection Research (DZIF), Partner site Hamburg-Lübeck-Borstel-Riems, Hamburg, Germany., Langeneckert AE; Department of Virus Immunology, Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany., Hess LU; Department of Virus Immunology, Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany., Poch T; I. Department of Medicine, Center for Internal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany., Martrus G; Department of Virus Immunology, Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany; German Center for Infection Research (DZIF), Partner site Hamburg-Lübeck-Borstel-Riems, Hamburg, Germany., Garcia-Beltran WF; Ragon Institute of MGH, MIT, and Harvard, Cambridge, Massachusetts., Körner C; Department of Virus Immunology, Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany., Ziegler AE; Department of Virus Immunology, Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany., Richert L; Department of Virus Immunology, Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany; INSERM U1219, INRIA SISTM, Bordeaux University, Bordeaux, France., Oldhafer KJ; Department of General and Abdominal Surgery, Asklepios Hospital Barmbek, Semmelweis University of Medicine, Asklepios Campus, Hamburg, Germany., Schulze Zur Wiesch J; I. Department of Medicine, Section Infectious Diseases, University Medical Center Hamburg-Eppendorf, Hamburg, Germany., Schramm C; I. Department of Medicine, Center for Internal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany., Dandri M; I. Department of Medicine, Center for Internal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany., Herker E; Junior Research Group HCV Replication, Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany., Altfeld M; Department of Virus Immunology, Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany; German Center for Infection Research (DZIF), Partner site Hamburg-Lübeck-Borstel-Riems, Hamburg, Germany; Institute for Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. Electronic address: marcus.altfeld@leibniz-hpi.de.
Jazyk:	angličtina
Zdroj:	Gastroenterology [Gastroenterology] 2018 Nov; Vol. 155 (5), pp. 1366-1371.e3. Date of Electronic Publication: 2018 Jul 19.
DOI:	10.1053/j.gastro.2018.07.019
Abstrakt:	Killer-cell immunoglobulin-like receptors (KIRs) are transmembrane glycoproteins expressed by natural killer (NK) cells. Binding of KIR3DS1 to its recently discovered ligand, HLA-F, activates NK cells and has been associated with resolution of hepatitis C virus (HCV) infection. We investigated the mechanisms by which KIR3DS1 contributes to the antiviral immune response. Using cell culture systems, mice with humanized livers, and primary liver tissue from HCV-infected individuals, we found that the KIR3DS1 ligand HLA-F is up-regulated on HCV-infected cells, and that interactions between KIR3DS1 and HLA-F contribute to NK cell-mediated control of HCV. Strategies to promote interaction between KIR3DS1 and HLA-F might be developed for treatment of infectious diseases and cancer. (Copyright © 2018 AGA Institute. Published by Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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