The vast majority of previous studies point to the inward flow of cortical F actin at the CAN be as the main or even only driving force behind centripetal receptor chaos movement. On the basis of this observation and of the staining of the HAS been different antibodies, Dustin proposed that the IS is essentially a symmetric model of the actin cytoskeleton at the top of a moving cell, where the dSMAC corresponds to the lamellipodium and the pSMAC corresponds to the lamellum. Implicit in this evaluation, therefore, is that the centripetal movement contact us of receptor clusters may well be influenced by a mixture of the driving force provided by polymerization based actin retrograde actin movement in the LP and the pulling force provided by myosin II based contraction of transverse actin bundles within the LM. Regarding the possible role of myosin II in the centripetal transportation of TCR MCs, an early study using blebbistatin to inhibit myosin II suggested the myosin is not needed for IS development. In contrast, a subsequent review applying both BB and RNA interference knock-down of myosin IIA noted a dramatic inhibition of inward TCR MC action, SMAC creation, and IS balance. Though effective in many features, this study did not image the character of F actin or myosin II, determine the effect of myosin Meristem II inhibition on the rate of actin move, define the organization of F actin within the LM/pSMAC, or identify the site of action of myosin II within the IS. More over, it didn’t parse out the relative contributions produced by actin retrograde movement and myosin II based contraction for the centripetal transport of TCR MCs. Armed with a novel reporter for F actin, we sought here to address these and related unresolved questions about the role of the actin cytoskeleton in formation. 1 Jurkat T cells activated by Doxorubicin structure glass supported planar lipid bilayers containing ICAM 1 and anti CD3 antibody. Anti CD3 antibody labeled with rhodamine X and attached to biotinylated fats in the bilayer via a streptavidin link distributes evenly in bilayers. Furthermore, usage of fluorescence recovery after photobleaching to measure the lateral mobility of ICAM 1 described with Alexa 647 and connected to the bilayer via nitrilotriacetic p conjugated lipids indicated the lipids in these bilayers are calming freely and evenly. Finally, after 5 min of involvement with the bilayer, the great majority of Jurkat T cells formed the main accumulation of TCR MCs, as inferred from the distribution of the anti CD3 antibody in the bilayer, and the peripheral accumulation of the integrin LFA 1, as inferred from the distribution of ICAM 1 in the bilayer, that is characteristic of the bulls eye patterned IS formed by primary T cells destined to bilayers containing peptide MHC.