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CXCR4 signaling and function require the expression of the IgD-class B-cell antigen receptor

MPG-Autoren

Becker,  Martin
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;
BIOSS Centre for Biological Signaling Studies. University Freiburg;
Department of Molecular Immunology, Institute of Biology III, University of Freiburg;

Reth,  Michael
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;
BIOSS Centre for Biological Signaling Studies. University Freiburg;
Department of Molecular Immunology, Institute of Biology III, University of Freiburg;

Maity,  Palash C.
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;
BIOSS Centre for Biological Signaling Studies. University Freiburg;
Department of Molecular Immunology, Institute of Biology III, University of Freiburg;

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Zitation

Becker, M., Hobeika, E., Jumaa, H., Reth, M., & Maity, P. C. (2017). CXCR4 signaling and function require the expression of the IgD-class B-cell antigen receptor. Proceedings of the National Academy of Sciences of the United States of America, 114, 5231-5236. doi:10.1073/pnas.1621512114.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-002E-85C8-7
Zusammenfassung
Mature B cells coexpress both IgM and IgD B-cell antigen receptor (BCR) classes, which are organized on the cell surface in distinct protein islands. The specific role of the IgD-BCR is still enigmatic, but it is colocalized with several other receptors on the B-cell surface, including the coreceptor CD19. Here, we report that the chemokine receptor CXCR4 is also found in proximity to the IgD-BCR. Furthermore, B cells from IgD-deficient mice show defects in CXCL12-mediated CXCR4 signaling and B-cell migration, whereas B cells from IgM-deficient mice are normal in this respect. CXCR4 activation results in actin cytoskeleton remodeling and PI3K/Akt and Erk signaling in an IgD-BCR-dependent manner. The defects in CXCR4 signaling in IgD-deficient B cells can be overcome by anti-CD19 antibody stimulation that also increases CXCL12-mediated B-cell migration of normal B cells. These results show that the IgD-BCR, CD19, and CXCR4 are not only colocalized at nanometer distances but are also functionally connected, thus providing a unique paradigm of receptor signaling cross talk and function.