Inhibitory killer cell immunoglobulin-like receptors strengthen CD8 + T cell-mediated control of HIV-1, HCV, and HTLV-1.

Autor:	Boelen L; Department of Medicine, Imperial College London, London, UK., Debebe B; Department of Medicine, Imperial College London, London, UK., Silveira M; Department of Medicine, Imperial College London, London, UK.; Faculty of Engineering, São Paulo State University-UNESP, São Paulo, Brazil., Salam A; Institute for Infection and Immunity, St. George's, University of London, London, UK., Makinde J; International AIDS Vaccine Initiative Human Immunology Laboratory, London, UK., Roberts CH; Clinical Research Department, London School of Hygiene and Tropical Medicine, London, UK., Wang ECY; Division of Infection and Immunity, Cardiff University School of Medicine, Cardiff, UK., Frater J; Nuffield Department of Medicine, University of Oxford, Oxford, UK.; Oxford NIHR Biomedical Research Centre, Oxford, UK., Gilmour J; International AIDS Vaccine Initiative Human Immunology Laboratory, London, UK., Twigger K; Department of Medicine, Imperial College London, London, UK., Ladell K; Division of Infection and Immunity, Cardiff University School of Medicine, Cardiff, UK., Miners KL; Division of Infection and Immunity, Cardiff University School of Medicine, Cardiff, UK., Jayaraman J; Immunology Division, Department of Pathology, University of Cambridge, Cambridge, UK., Traherne JA; Immunology Division, Department of Pathology, University of Cambridge, Cambridge, UK., Price DA; Division of Infection and Immunity, Cardiff University School of Medicine, Cardiff, UK., Qi Y; Cancer and Inflammation Program, Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, USA., Martin MP; Cancer and Inflammation Program, Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, USA., Macallan DC; Institute for Infection and Immunity, St. George's, University of London, London, UK., Thio CL; Johns Hopkins University, Baltimore, MD, USA., Astemborski J; Johns Hopkins University, Baltimore, MD, USA., Kirk G; Johns Hopkins University, Baltimore, MD, USA., Donfield SM; Rho, Chapel Hill, NC, USA., Buchbinder S; San Francisco Department of Public Health, San Francisco, CA, USA., Khakoo SI; Faculty of Medicine, University of Southampton, Southampton, UK., Goedert JJ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA., Trowsdale J; Immunology Division, Department of Pathology, University of Cambridge, Cambridge, UK., Carrington M; Cancer and Inflammation Program, Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, USA.; Ragon Institute of MGH, MIT and Harvard, Boston, MA, USA., Kollnberger S; Division of Infection and Immunity, Cardiff University School of Medicine, Cardiff, UK., Asquith B; Department of Medicine, Imperial College London, London, UK. b.asquith@imperial.ac.uk.
Jazyk:	angličtina
Zdroj:	Science immunology [Sci Immunol] 2018 Nov 09; Vol. 3 (29).
DOI:	10.1126/sciimmunol.aao2892
Abstrakt:	Killer cell immunoglobulin-like receptors (KIRs) are expressed predominantly on natural killer cells, where they play a key role in the regulation of innate immune responses. Recent studies show that inhibitory KIRs can also affect adaptive T cell-mediated immunity. In mice and in human T cells in vitro, inhibitory KIR ligation enhanced CD8 + T cell survival. To investigate the clinical relevance of these observations, we conducted an extensive immunogenetic analysis of multiple independent cohorts of HIV-1-, hepatitis C virus (HCV)-, and human T cell leukemia virus type 1 (HTLV-1)-infected individuals in conjunction with in vitro assays of T cell survival, analysis of ex vivo KIR expression, and mathematical modeling of host-virus dynamics. Our data suggest that functional engagement of inhibitory KIRs enhances the CD8 + T cell response against HIV-1, HCV, and HTLV-1 and is a significant determinant of clinical outcome in all three viral infections. (Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.)
Databáze:	MEDLINE
Externí odkaz:	Zobrazit plný text záznamu