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      Neutrophil migration in infection and wound repair: going forward in reverse

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          Abstract

          Neutrophil migration and its role during inflammation has been the focus of increased interest in the past decade. Advances in live imaging and the use of new model systems have helped to uncover the behaviour of neutrophils in injured and infected tissues. Although neutrophils were considered to be short-lived effector cells that undergo apoptosis in damaged tissues, recent evidence suggests that neutrophil behaviour is more complex and, in some settings, neutrophils might leave sites of tissue injury and migrate back into the vasculature. The role of reverse migration and its contribution to resolution of inflammation remains unclear. Here, we discuss the different cues within tissues that mediate neutrophil forward and reverse migration in response to injury or infection, and the implications of these mechanisms to human disease.

          TOC blurb

          Neutrophils follow a multitude of signals to reach sites of injury or infection. Understanding how this occurs and what the fate of these neutrophils is provides insight into how immune responses are controlled and chronic inflammation avoided. Here, the authors describe the movement of neutrophils during inflammation.

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          Author and article information

          Journal
          101124169
          27017
          Nat Rev Immunol
          Nat. Rev. Immunol.
          Nature reviews. Immunology
          1474-1733
          1474-1741
          15 February 2017
          27 May 2016
          27 March 2017
          : 16
          : 6
          : 378-391
          Affiliations
          [1 ]Department of Medical Microbiology and Immunology, University of Wisconsin, Madison, Wisconsin 53706, USA
          [2 ]Department of Pediatrics, University of Wisconsin, Madison, Wisconsin 53706, USA
          Author notes
          Correspondence to A.H. huttenlocher@ 123456wisc.edu
          [*]

          Equal contribution

          Article
          PMC5367630 PMC5367630 5367630 nihpa851307
          10.1038/nri.2016.49
          5367630
          27231052
          f9189b3a-7a66-46d6-a82e-30a05021ebd5
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