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Fig. 2. Cellular mechanism for the inside-out activation of integrins. Following BCR stimulation with antigen on the surface of an APC, BCR-antigen microclusters form throughout the area of contact. These microclusters act as the sites for microsignalosome assembly and recruit molecules such as Syk, Vav, CD19, PLC
2 (Weber et al., 2008) and PI3K (D. Depoil and F.D.B., unpublished data). We propose that these microsignalosomes provide a favourable environment for the activation of small GTPases such as Rac2 (shown in grey), which in turn mediate reorganisation of the cytoskeleton and activation of integrin-mediated B-cell adhesion. Enhanced adhesion and signalling through the BCR allow for propagation of the B-cell spreading response. We suggest that microsignalosomes are transported from the periphery to the cSMAC by centripetal retrograde actin flow in a manner similar to that recently observed in T cells (Kaizuka et al., 2007). The presence of activated integrins during spreading promotes B-cell adhesion, which stimulates the generation of further microsignalosomes and ultimately facilitates the activation of B cells.
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