Transitional B cells commit to marginal zone B cell fate by Taok3-mediated surface expression of ADAM10.
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Hammad H
VIB Inflammation Research Center, Ghent University, Ghent, Belgium.
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Vanderkerken M
VIB Inflammation Research Center, Ghent University, Ghent, Belgium.
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Pouliot P
VIB Inflammation Research Center, Ghent University, Ghent, Belgium.
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Deswarte K
VIB Inflammation Research Center, Ghent University, Ghent, Belgium.
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Toussaint W
VIB Inflammation Research Center, Ghent University, Ghent, Belgium.
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Vergote K
VIB Inflammation Research Center, Ghent University, Ghent, Belgium.
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Vandersarren L
VIB Inflammation Research Center, Ghent University, Ghent, Belgium.
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Janssens S
VIB Inflammation Research Center, Ghent University, Ghent, Belgium.
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Ramou I
VIB Inflammation Research Center, Ghent University, Ghent, Belgium.
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Savvides SN
VIB Inflammation Research Center, Ghent University, Ghent, Belgium.
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Haigh JJ
VIB Inflammation Research Center, Ghent University, Ghent, Belgium.
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Hendriks R
Department of Pulmonary Medicine, Erasmus Medical Center, Rotterdam, the Netherlands.
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Kopf M
Institute for Molecular Health Sciences, ETH, Zürich, Switzerland.
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Craessaerts K
VIB Center for Brain and Disease, VIB, Leuven, Belgium.
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de Strooper B
VIB Center for Brain and Disease, VIB, Leuven, Belgium.
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Kearney JF
Department of Microbiology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
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Conrad DH
Center for Clinical and Translational Research, Virginia Commonwealth University, Richmond, Virginia, USA.
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Lambrecht BN
VIB Inflammation Research Center, Ghent University, Ghent, Belgium.
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Published in:
- Nature immunology. - 2017
English
Notch2 and B cell antigen receptor (BCR) signaling determine whether transitional B cells become marginal zone B (MZB) or follicular B (FoB) cells in the spleen, but it is unknown how these pathways are related. We generated Taok3-/- mice, lacking the serine/threonine kinase Taok3, and found cell-intrinsic defects in the development of MZB but not FoB cells. Type 1 transitional (T1) B cells required Taok3 to rapidly respond to ligation by the Notch ligand Delta-like 1. BCR ligation by endogenous or exogenous ligands induced the surface expression of the metalloproteinase ADAM10 on T1 B cells in a Taok3-dependent manner. T1 B cells expressing surface ADAM10 were committed to becoming MZB cells in vivo, whereas T1 B cells lacking expression of ADAM10 were not. Thus, during positive selection in the spleen, BCR signaling causes immature T1 B cells to become receptive to Notch ligands via Taok3-mediated surface expression of ADAM10.
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Language
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Open access status
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green
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Persistent URL
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https://folia.unifr.ch/global/documents/77558
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