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PLoS ONE. CCR2 Defines a Distinct Population of NK Cells and Mediates Their Migration during Influenza Virus Infection in Mice

Giuseppe

Emeritus
[Source: PLoS ONE, full page: (LINK). Abstract, edited.]

CCR2 Defines a Distinct Population of NK Cells and Mediates Their Migration during Influenza Virus Infection in Mice


Mary J. G. van Helden, Dietmar M. W. Zaiss<SUP>*</SUP>, Alice J. A. M. Sijts<SUP>*</SUP>
<SUP></SUP>
Department of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, University of Utrecht, Utrecht, The Netherlands



Abstract

Natural killer (NK) cells are innate lymphocytes that play an important role in control of viral infections. We recently showed that intranasal infection of mice with influenza virus induced the accumulation of NK cells in the airways. NK cells however did not proliferate in the airways or in the draining lymph node, but in the bone marrow mainly. As also monocyte-precursors undergo vigorous proliferation in the bone marrow (BM) during infections and then egress CCR2-dependently, we decided to determine the role of CCR2 in NK cell migration during intranasal influenza virus infection. We show that a unique population of NK cells in the BM expressed CCR2 and that monocyte chemotactic protein-1 (MCP-1), one of the CCR2 ligands, was produced in the airways of influenza virus infected mice. Analysis of BM chimeric mice reconstituted with a mix of wild-type (wt) and CCR2-deficient BM cells showed that upon influenza virus infection, a significantly lower proportion of CCR2-deficient than wt NK cells was recovered from the bronchoalveolar lavage (BAL). Taken together, our data demonstrate that during influenza virus infection a proportion of NK cells migrate in a CCR2-dependent fashion.



Citation: van Helden MJG, Zaiss DMW, Sijts AJAM (2012) CCR2 Defines a Distinct Population of NK Cells and Mediates Their Migration during Influenza Virus Infection in Mice. PLoS ONE 7(12): e52027. doi:10.1371/journal.pone.0052027

Editor: Ali A. Ashkar, McMaster University, Canada

Received: September 10, 2012; Accepted: November 13, 2012; Published: December 13, 2012

Copyright: ? 2012 van Helden et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: Top Institute Pharma grant T4-214, URL: http://www.tipharma.com/and Wellcome Trust grant WT085733MA, URL: http://www.wellcome.ac.uk/. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have declared that no competing interests exist.

* E-mail: d.zaiss@uu.nl (DMWZ); e.j.a.m.sijts@uu.nl (AJAMS)
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