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Immunity. 2010 Feb 26;32(2):187-99. doi: 10.1016/j.immuni.2009.12.005. Epub 2010 Feb 18.

The membrane skeleton controls diffusion dynamics and signaling through the B cell receptor.

Author information

1
Lymphocyte Interaction Laboratory, London Research Institute, Cancer Research UK, 44 Lincoln's Inn Fields, London WC2A 3PX, UK.

Abstract

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 Igbeta 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.

PMID:
20171124
PMCID:
PMC2984614
DOI:
10.1016/j.immuni.2009.12.005
[Indexed for MEDLINE]
Free PMC Article

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