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Nat Methods. 2015 May;12(5):445-52. doi: 10.1038/nmeth.3322. Epub 2015 Mar 16.

Catchup: a mouse model for imaging-based tracking and modulation of neutrophil granulocytes.

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Institute for Experimental Immunology and Imaging, University Hospital, University Duisburg-Essen, Essen, Germany.
Institute of Experimental Immunology, Friedrich-Wilhelms-Universität Bonn, Bonn, Germany.
Institute for Molecular Medicine, Johannes Gutenberg-University of Mainz, Mainz, Germany.
Institute of Molecular and Clinical Immunology, Otto von Guericke University, Magdeburg, Germany.
Department of Otorhinolaryngology, University Hospital, University Duisburg-Essen, Essen, Germany.
Department of Biology, Institute of Genetics, University of Erlangen-Nuremberg, Erlangen, Germany.
1] Institute of Molecular and Clinical Immunology, Otto von Guericke University, Magdeburg, Germany. [2] Department of Immune Control, Helmholtz Centre for Infection Research (HZI), Braunschweig, Germany.
Department of Hematology, University Hospital, West German Cancer Center (WTZ), University Duisburg-Essen, Essen, Germany.


Neutrophil granulocyte biology is a central issue of immunological research, but the lack of animal models that allow for neutrophil-selective genetic manipulation has delayed progress. By modulating the neutrophil-specific locus Ly6G with a knock-in allele expressing Cre recombinase and the fluorescent protein tdTomato, we generated a mouse model termed Catchup that exhibits strong neutrophil specificity. Transgene activity was found only in very few eosinophils and basophils and was undetectable in bone marrow precursors, including granulomonocytic progenitors (GMPs). Cre-mediated reporter-gene activation allowed for intravital two-photon microscopy of neutrophils without adoptive transfer. Homozygous animals were Ly6G deficient but showed normal leukocyte cellularity in all measured organs. Ly6G-deficient neutrophils were functionally normal in vitro and in multiple models of sterile or infectious inflammation in vivo. However, Cre-mediated deletion of FcγRIV in neutrophils reduced the cells' recruitment to immune-complex-mediated peritonitis, suggesting a cell-intrinsic role for activating Fc receptors in neutrophil trafficking.

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