| Literature DB >> 30031767 |
Sebastian Lunemann1, Anja Schöbel2, Janine Kah3, Pia Fittje1, Angelique Hölzemer4, Annika E Langeneckert1, Leonard U Hess1, Tobias Poch3, Gloria Martrus5, Wilfredo F Garcia-Beltran6, Christian Körner1, Annerose E Ziegler1, Laura Richert7, Karl J Oldhafer8, Julian Schulze Zur Wiesch9, Christoph Schramm3, Maura Dandri3, Eva Herker2, Marcus Altfeld10.
Abstract
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.Entities:
Keywords: Antiviral Immune Response; Human Leukocyte Antigen; Immunity; Regulation
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Year: 2018 PMID： 30031767 DOI： 10.1053/j.gastro.2018.07.019
Source DB: PubMed Journal: Gastroenterology ISSN： 0016-5085 Impact factor: 22.682