期刊
IMMUNITY
卷 32, 期 2, 页码 187-199出版社
CELL PRESS
DOI: 10.1016/j.immuni.2009.12.005
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资金
- Cancer Research UK
- Royal Society Wolfson Research Merit Award
- National Science and Engineering Research Council of Canada
- Mathematics in Technology and Complex Systems National Centre of Excellence, Canada
Early events of B cell activation after B cell receptor (BCR) triggering have been well characterized. However, little is known about the steady state of the BCR on the cell surface. Here, we simultaneously visualize single BCR particles and components of the membrane skeleton. We show that an ezrin- and actin-defined network influenced steady-state BCR diffusion by creating boundaries that restrict BCR diffusion. We identified the intracellular domain of Ig beta as important in mediating this restriction in diffusion. Importantly, alteration of this network was sufficient to induce robust intracellular signaling and concomitant increase in BCR mobility. Moreover, by using B cells deficient in key signaling molecules, we show that this signaling was most probably initiated by the BCR. Thus, our results suggest the membrane skeleton plays a crucial function in controlling BCR dynamics and thereby signaling, in a way that could be important for understanding tonic signaling necessary for B cell development and survival.
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