CD19 and BAFF‐R can signal to promote B‐cell survival in the absence of Syk |
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| Authors: | Vasiliki Anastasopoulou Roland Pohlmeyer Simon Altmeier Ameera Alsadeq Marc‐Werner Dobenecker Roberta Pelanda Michael Reth |
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| Institution: | 1. Institute of Immunology, Charité Campus Buch, Berlin, Germany;2. Max‐Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany;3. Institute of Mircobiology, Swiss Federal Institute of Technology, ETH Zurich, Zurich, Switzerland;4. Department of General Pediatrics, University Medical Center Schleswig‐Holstein, Kiel, Germany;5. Laboratory of Immune Cell Epigenetics and Signaling, The Rockefeller University, New York, NY, USA;6. Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO, USA;7. Department of Molecular Immunology, BioIII, Faculty of Biology, Albert‐Ludwigs‐Universit?t Freiburg, Freiburg, Germany;8. BIOSS, Centre For Biological Signaling Studies, University of Freiburg, Freiburg, Germany |
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| Abstract: | 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. |
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| Keywords: | BAFF receptor B‐cell antigen receptor CD19 mb1‐CreERT2 Syk |
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