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The dissociation activation model of B cell antigen receptor triggering

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Yang,  Jianying
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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Reth,  Michael
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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Citation

Yang, J., & Reth, M. (2010). The dissociation activation model of B cell antigen receptor triggering. FEBS Letters, 584, 4872-4877.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002B-8EF4-1
Abstract
To detect its cognate antigen, each B lymphocyte contains up to 120000 B cell antigen receptor (BCR) complexes on its cell surface. How these abundant receptors remain silent on resting B cells and how they can be activated by a molecularly diverse set of ligands is poorly understood. The antigen-specific activation of the BCR is currently explained by the cross-linking model (CLM). This model predicts that the many BCR complexes on the surface of a B cell are dispersed signalling-inert monomers and that it is BCR dimerization that initiates signalling from the receptor. The finding that the BCR forms auto-inhibited oligomers on the surface of resting B cells falsifies these predictions of the CLM. We propose the dissociation activation model (DAM), which fits better with the existing body of experimental data.