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The dissociation activation model of B cell antigen receptor triggering
Author(s) -
Yang Jianying,
Reth Michael
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.09.045
Subject(s) - breakpoint cluster region , receptor , b cell receptor , antigen , microbiology and biotechnology , signalling , chemistry , b cell , cell , t cell receptor , dissociation (chemistry) , biophysics , biology , t cell , immunology , biochemistry , antibody , immune system
To detect its cognate antigen, each B lymphocyte contains up to 120 000 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.