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The binding of LFA-1 on a T cell's surface is a critical step for intravascular adhesion and cell migration. Volkov et al. report that, in the T cell's uropod, LFA-1 activates the PKC-(I) (green) pathway to trigger the polymer-ization of tubulin (red) and there-by initiate the migratory capacity of the cells. Blue, nuclei; yellow-orange, colocalization of PKC-(I) and tubulin. Fluorescent image taken by Y. Volkov with an 100x oil immersion lens on a Nikon TE300 microscope and Photometrics-cooled CCD camera.
The events that enable polarization of T cells and migration across the vasculature to the target are largely unknown. New evidence suggests that PKC-β(I) may be pivotal in controlling this process.
Our current understanding of lymphocyte migration across the endothelium includes four steps: attachment, rolling, arrest and diapedesis. New evidence suggests the involvement of another step, chemorheotaxis.
T cells, move over. B cells are now reported, in a recent paper in Nature, to have their own immunological synapses with APCs. Only this time the antigen is whole and B cells don't keep it to themselves.
Genetic ablation experiments have shown that Vav is critical for TCR signaling. Evidence is now emerging that the Vav family of signaling molecules play a critical role in antigen receptor signaling in B cells as well as in T cells.
Multiple error-prone DNA polymerase appear to contribute to immunoglobulin somatic hypermutation. Genetic and biochemical data now indicate that DNA polymerase η may be responsible for the generation of some of the strand-biased hotspot A mutations in the immunoglobulin loci.