| Literature DB >> 28068307 |
Hamida Hammad1,2, Matthias Vanderkerken1,2, Philippe Pouliot1,2, Kim Deswarte1,2, Wendy Toussaint1,2, Karl Vergote1,2, Lana Vandersarren1,2, Sophie Janssens1,2, Ioanna Ramou1,3, Savvas N Savvides1,3, Jody J Haigh1, Rudi Hendriks4, Manfred Kopf5, Katleen Craessaerts6,7, Bart de Strooper6,7, John F Kearney8, Daniel H Conrad9, Bart N Lambrecht1,2,4.
Abstract
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.Entities:
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Year: 2017 PMID： 28068307 DOI： 10.1038/ni.3657
Source DB: PubMed Journal: Nat Immunol ISSN： 1529-2908 Impact factor: 25.606