 area dynamics between cell types (Dobereiner et al., 2006; Sims et al., 2007). Our collaborative studies revealed that the outer edge of the immunological synapse displayed an evolutionarily conserved dynamic pattern of movement referred to as contractile oscillations (Fig 1). This is thought to emerge from cycles of F-actin polymerization and myosin II dependent contraction that periodically pull the membrane protrusion up and back. This is an excellent way to test the mechanical properties of the surface on which cells are interacting. This protrusion and retraction cycle then propagates as a wave around the entire periphery of the cell. These experiments provided strong quantitative evidence the periphery of primary mouse T cells forming synapses or kinapses on planar bilayers with MHC-pepide complexes, ICAM-1 and CD80 form a radial lamellipodium. More recently, Vale and my lab used speckle microscopy to explicitly demonstrate centripetal actin flow in the dSMAC and pSMAC regions (Kaizuka et al., 2007). This F-actin flow is a consequence of the polymerization of F-actin at the protruding edge, which is pushed backwards because the outer edge advances more slowly than actin is added to the growing filament ends. TCR microclusters are transported at about 40% of the speed of the F-actin in the lamellipodium. This suggests that the microclusters bind and dissociate from the actin network. This notion is also supported by studies showing that TCR clusters can navigate around barriers placed in planar bilayers by nanofabrication methods (DeMond et al., 2008). The ability to move around the barriers appears to depend upon periods of transport punctuated by diffusive movement, which allows the microcluster to make progress around diagonal barriers. TCR microcluster transport, contractile oscillations and centripetal F-actin flow support the model that immunological synapses are based on maintaining a radially symmetrical lamellipodium-the same structure Kupfer described as a dSMAC (Freiberg et al., 2002). The dSMAC 