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dc.contributor.authorKleinholz, Corinna L
dc.contributor.authorRiek-Burchardt, Monika
dc.contributor.authorSeiß, Elena A
dc.contributor.authorAmore, Jonas
dc.contributor.authorGintschel, Patricia
dc.contributor.authorPhilipsen, Lars
dc.contributor.authorBousso, Philippe
dc.contributor.authorRelja, Borna
dc.contributor.authorSchraven, Burkhart
dc.contributor.authorHandschuh, Juliane
dc.contributor.authorMohr, Juliane
dc.contributor.authorMüller, Andreas J
dc.date.accessioned2021-09-08T13:27:15Z
dc.date.available2021-09-08T13:27:15Z
dc.date.issued2021-07-23
dc.identifier.citationSci Rep. 2021 Jul 23;11(1):15071. doi: 10.1038/s41598-021-94425-9.en_US
dc.identifier.pmid34302006
dc.identifier.doi10.1038/s41598-021-94425-9
dc.identifier.urihttp://hdl.handle.net/10033/623019
dc.description.abstractNeutrophils represent one of the first immune cell types recruited to sites of infection, where they can control pathogens by phagocytosis and cytotoxic mechanisms. Intracellular pathogens such as Leishmania major can hijack neutrophils to establish an efficient infection. However the dynamic interactions of neutrophils with the pathogen and other cells at the site of the infection are incompletely understood. Here, we have investigated the role of Ly6G, a homolog of the human CD177 protein, which has been shown to interact with cell adhesion molecules, and serves as a bona fide marker for neutrophils in mice. We show that Ly6G deficiency decreases the initial infection rate of neutrophils recruited to the site of infection. Although the uptake of L. major by subsequently recruited monocytes was tightly linked with the concomitant uptake of neutrophil material, this process was not altered by Ly6G deficiency of the neutrophils. Instead, we observed by intravital 2-photon microscopy that Ly6G-deficient neutrophils entered the site of infection with delayed initial recruitment kinetics. Thus, we conclude that by promoting neutrophils' ability to efficiently enter the site of infection, Ly6G contributes to the early engagement of intracellular pathogens by the immune system.en_US
dc.language.isoenen_US
dc.publisherNPGen_US
dc.rightsAttribution 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.titleLy6G deficiency alters the dynamics of neutrophil recruitment and pathogen capture during Leishmania major skin infection.en_US
dc.typeArticleen_US
dc.identifier.eissn2045-2322
dc.contributor.departmentHZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.en_US
dc.identifier.journalScientific reportsen_US
dc.source.volume11
dc.source.issue1
dc.source.beginpage15071
dc.source.endpage
refterms.dateFOA2021-09-08T13:27:15Z
dc.source.journaltitleScientific reports
dc.source.countryEngland


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Attribution 4.0 International
Except where otherwise noted, this item's license is described as Attribution 4.0 International