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ID 112441
著者
Gamrekelashvili, Jaba Hannover Medical School
Giagnorio, Roberto Hannover Medical School
Jussofie, Jasmin Hannover Medical School
Soehnlein, Oliver Ludwig-Maximilians-University|Amsterdam University|German Centre for Cardiovascular Research
Duchene, Johan Ludwig-Maximilians-University
Briseño, Carlos G. Washington University in St Louis
Ramasamy, Saravana K. Max Planck Institute for Molecular Biomedicine
Krishnasamy, Kashyap Hannover Medical School
Limbourg, Anne Hannover Medical School
Häger, Christine Hannover Medical School
Kapanadze, Tamar Hannover Medical School
Hinkel, Rabea Ludwig-Maximilians-University|Technical University of Munich
Radtke, Freddy Ecole Polytechnique Fédérale de Lausanne
Strobl, Lothar J. German Research Center for Environment and Health (GmbH)
Zimber-Strobl, Ursula German Research Center for Environment and Health (GmbH)
Napp, L. Christian Hannover Medical School
Bauersachs, Johann Hannover Medical School
Haller, Hermann Hannover Medical School
Kupatt, Christian Ludwig-Maximilians-University|Technical University of Munich
Murphy, Kenneth M. Washington University in St Louis
Adams, Ralf H. Max Planck Institute for Molecular Biomedicine
Weber, Christian Ludwig-Maximilians-University|Cardiovascular Research Institute Maastricht (CARIM)
Limbourg, Florian P. Hannover Medical School
資料タイプ
学術雑誌論文
抄録
A population of monocytes, known as Ly6Clo monocytes, patrol blood vessels by crawling along the vascular endothelium. Here we show that endothelial cells control their origin through Notch signalling. Using combinations of conditional genetic deletion strategies and cell-fate tracking experiments we show that Notch2 regulates conversion of Ly6Chi monocytes into Ly6Clo monocytes in vivo and in vitro, thereby regulating monocyte cell fate under steady-state conditions. This process is controlled by Notch ligand delta-like 1 (Dll1) expressed by a population of endothelial cells that constitute distinct vascular niches in the bone marrow and spleen in vivo, while culture on recombinant DLL1 induces monocyte conversion in vitro. Thus, blood vessels regulate monocyte conversion, a form of committed myeloid cell fate regulation.
掲載誌名
Nature Communications
ISSN
20411723
cat書誌ID
AA12645905
出版者
Springer Nature
7
開始ページ
12597
発行日
2016-08-31
備考
Supplementary Information : ncomms_7_12597_s1.pdf
Corrigendum : https://doi.org/10.1038/ncomms15486
権利情報
This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
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出版社版DOI
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フルテキストファイル
言語
eng
著者版フラグ
出版社版
部局
医学系