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CD161 defines a functionally distinct subset of pro-inflammatory natural killer cells

Lookup NU author(s): Dr Lucy Walker

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This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).


Abstract

© 2018 Kurioka, Cosgrove, Simoni, van Wilgenburg, Geremia, Björkander, Sverremark-Ekström, Thurnheer, Günthard, Khanna, The Swiss HIV Cohort Study, Oxford IBD Cohort Investigators, Walker, Arancibia-Cárcamo, Newell, Willberg and Klenerman.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.


Publication metadata

Author(s): Kurioka A, Cosgrove C, Simoni Y, van Wilgenburg B, Geremia A, Bjorkander S, Sverremark-Ekstrom E, Thurnheer C, Gunthard HF, Khanna N, The Swiss HIV Cohort Study, Oxford IBD Cohort Investigators, Walker LJ, Arancibia-Carcamo CV, Newell EW, Willberg CB, Klenerman P

Publication type: Article

Publication status: Published

Journal: Frontiers in Immunology

Year: 2018

Volume: 9

Online publication date: 09/04/2018

Acceptance date: 23/02/2018

Date deposited: 06/06/2018

ISSN (electronic): 1664-3224

Publisher: Frontiers Research Foundation

URL: https://doi.org/10.3389/fimmu.2018.00486

DOI: 10.3389/fimmu.2018.00486


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