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CD19 and BAFF-R can signal to promote B-cell survival in the absence of Syk

MPG-Autoren
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Hobeika,  Elias
BIOSS, Centre for Biological Signaling Studies, University of Freiburg;
Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Zerdoun Levit,  Ella
Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Pohlmeyer,  Roland
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

/persons/resource/persons191285

Reth,  Michael
BIOSS, Centre for Biological Signaling Studies, University of Freiburg;
Department of Molecular Immunology, BioIII, Faculty of Biology, Albert-Ludwigs-Universität Freiburg;
Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Zitation

Hobeika, E., Zerdoun Levit, E., Anastasopoulou, V., Pohlmeyer, R., Altmeier, S., Alsedeq, A., et al. (2015). CD19 and BAFF-R can signal to promote B-cell survival in the absence of Syk. The EMBO Journal, 34, 925-939.


Zitierlink: https://hdl.handle.net/someHandle/test/escidoc:902507
Zusammenfassung
The development and function of B lymphocytes is regulated by numerous signaling pathways, some emanating from the B-cell antigen receptor (BCR). The spleen tyrosine kinase (Syk) plays a central role in the activation of the BCR, but less is known about its contribution to the survival and maintenance of mature B cells. We generated mice with an inducible and B-cell-specific deletion of the Syk gene and found that a considerable fraction of mature Syk-negative B cells can survive in the periphery for an extended time. Syk-negative B cells are defective in BCR, RP105 and CD38 signaling but still respond to an IL-4, anti-CD40, CpG or LPS stimulus. Our in vivo experiments show that Syk-deficient B cells require BAFF receptor and CD19/PI3K signaling for their long-term survival. These studies also shed a new light on the signals regulating the maintenance of the normal mature murine B-cell pool.