(1) Kurioka A (2) Cosgrove C (3) Simoni Y (4) van Wilgenburg B (5) Geremia A (6) Bjšrkander S (7) Sverremark-Ekstršm E (8) Thurnheer C (9) GŸnthard HF (10) Khanna N (11) Walker LJ (12) Arancibia-C‡rcamo CV (13) Newell EW (14) Willberg CB (15) Klenerman P

Frontiers in immunology | Free PMC Article

CD161 is a C-type lectin-like receptor expressed on the majority of natural killer (NK) cells; however, the significance of CD161 expression on NK cells has not been comprehensively investigated. Recently, we found that CD161 expression identifies a transcriptional and innate functional phenotype that is shared across various T cell populations. Using mass cytometry and microarray experiments, we demonstrate that this functional phenotype extends to NK cells. CD161 marks NK cells that have retained the ability to respond to innate cytokines during their differentiation, and is lost upon cytomegalovirus-induced maturation in both healthy and human immunodeficiency virus (HIV)-infected patients. These pro-inflammatory NK cells are present in the inflamed lamina propria where they are enriched for integrin CD103 expression. Thus, CD161 expression identifies NK cells that may contribute to inflammatory disease pathogenesis and correlates with an innate responsiveness to cytokines in both T and NK cells.

Author Info: (1) The Peter Medawar Building for Pathogen Research, University of Oxford, Oxford, United Kingdom. (2) Ragon Institute of Massachusetts General Hospital, Harvard University, Massa

Author Info: (1) The Peter Medawar Building for Pathogen Research, University of Oxford, Oxford, United Kingdom. (2) Ragon Institute of Massachusetts General Hospital, Harvard University, Massachusetts Institute of Technology, Cambridge, MA, United States. (3) Agency for Science, Technology and Research (ASTAR), Singapore Immunology Network (SIgN), Singapore, Singapore. (4) The Peter Medawar Building for Pathogen Research, University of Oxford, Oxford, United Kingdom. (5) Translational Gastroenterology Unit, Experimental Medicine Division, University of Oxford, John Radcliffe Hospital, Oxford, United Kingdom. (6) Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden. (7) Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden. (8) Division of Infectious Diseases, University Hospital Berne, University of Berne, Berne, Switzerland. (9) Division of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, University of Zurich, Zurich, Switzerland. Institute of Medical Virology, University of Zurich, Zurich, Switzerland. (10) Division of Infectious Diseases, University Hospital Basel, Basel, Switzerland. (11) Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom. (12) Translational Gastroenterology Unit, Experimental Medicine Division, University of Oxford, John Radcliffe Hospital, Oxford, United Kingdom. (13) Agency for Science, Technology and Research (ASTAR), Singapore Immunology Network (SIgN), Singapore, Singapore. (14) The Peter Medawar Building for Pathogen Research, University of Oxford, Oxford, United Kingdom. NIHR Biomedical Research Centre, University of Oxford, Oxford, United Kingdom. (15) The Peter Medawar Building for Pathogen Research, University of Oxford, Oxford, United Kingdom. NIHR Biomedical Research Centre, University of Oxford, Oxford, United Kingdom.

Citation: Front Immunol 2018 9:486 Epub04/09/2018

Link to PUBMED: http://www.ncbi.nlm.nih.gov/pubmed/29686665

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