Influenza A Virus Infection Induces Hyperresponsiveness in Human Lung Tissue-Resident and Peripheral Blood NK Cells

Show simple item record Scharenberg, Marlena Vangeti, Sindhu Kekäläinen, Eliisa Bergman, Per Al-Ameri, Mamdoh Johansson, Niclas Sonden, Klara Falck-Jones, Sara Färnert, Anna Ljunggren, Hans-Gustaf Michaelsson, Jakob Smed-Sörensen, Anna Marquardt, Nicole 2019-06-27T07:30:02Z 2019-06-27T07:30:02Z 2019-05-17
dc.identifier.citation Scharenberg , M , Vangeti , S , Kekäläinen , E , Bergman , P , Al-Ameri , M , Johansson , N , Sonden , K , Falck-Jones , S , Färnert , A , Ljunggren , H-G , Michaelsson , J , Smed-Sörensen , A & Marquardt , N 2019 , ' Influenza A Virus Infection Induces Hyperresponsiveness in Human Lung Tissue-Resident and Peripheral Blood NK Cells ' , Frontiers in Immunology , vol. 10 , 1116 .
dc.identifier.other PURE: 125374733
dc.identifier.other PURE UUID: eac4244a-44f0-4a46-8129-1ce6579b338f
dc.identifier.other WOS: 000468164800002
dc.identifier.other ORCID: /0000-0001-6045-108X/work/58954200
dc.description.abstract NK cells in the human lung respond to influenza A virus-(IAV-) infected target cells. However, the detailed functional capacity of human lung and peripheral blood NK cells remains to be determined in IAV and other respiratory viral infections. Here, we investigated the effects of IAV infection on human lung and peripheral blood NK cells in vitro and ex vivo following clinical infection. IAV infection of lung- and peripheral blood-derived mononuclear cells in vitro induced NK cell hyperresponsiveness to K562 target cells, including increased degranulation and cytokine production particularly in the CD56(bright)CD16(-) subset of NK cells. Furthermore, lung CD16(-) NK cells showed increased IAV-mediated but target cell-independent activation compared to CD16(+) lung NK cells or total NK cells in peripheral blood. IAV infection rendered peripheral blood NK cells responsive toward the normally NK cell-resistant lung epithelial cell line A549, indicating that NK cell activation during IAV infection could contribute to killing of surrounding non-infected epithelial cells. In vivo, peripheral blood CD56(dim)CD16(+) and CD56(bright)CD16(-) NK cells were primed during acute IAV infection, and a small subset of CD16(-) CD49a(+)CXCR3(+) NK cells could be identified, with CD49a and CXCR3 potentially promoting homing to and tissue-retention in the lung during acute infection. Together, we show that IAV respiratory viral infections prime otherwise hyporesponsive lung NK cells, indicating that both CD16(+) and CD16(-) NK cells including CD16(-)CD49a(+) tissue-resident NK cells could contribute to host immunity but possibly also tissue damage in clinical IAV infection. en
dc.format.extent 10
dc.language.iso eng
dc.relation.ispartof Frontiers in Immunology
dc.rights cc_by
dc.rights.uri info:eu-repo/semantics/openAccess
dc.subject human
dc.subject lung
dc.subject NK cells
dc.subject influenza A virus
dc.subject viral pathogenesis
dc.subject respiratory infections
dc.subject IMMUNE INJURY
dc.subject EXPRESSION
dc.subject IP-10
dc.subject ACTIVATION
dc.subject IL-15
dc.subject CXCR3
dc.subject H5N1
dc.subject 3111 Biomedicine
dc.subject 3121 General medicine, internal medicine and other clinical medicine
dc.title Influenza A Virus Infection Induces Hyperresponsiveness in Human Lung Tissue-Resident and Peripheral Blood NK Cells en
dc.type Article
dc.contributor.organization Department of Bacteriology and Immunology
dc.contributor.organization Immunobiology Research Program
dc.contributor.organization HUSLAB
dc.contributor.organization Medicum
dc.contributor.organization Research Programs Unit
dc.contributor.organization Helsinki University Hospital Area
dc.description.reviewstatus Peer reviewed
dc.relation.issn 1664-3224
dc.rights.accesslevel openAccess
dc.type.version publishedVersion

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