ch has also been referred to as a focal zone in migrating T cells (Smith et al., 2005). These zones are rich in adhesion sites and integrin binding adapter talin, which is also a marker of the pSMAC. T cell may arrest migration and form a stable synapse, or alternatively, they may continue to migrate and integrate signals on the move. This rapid migration during antigen recognition contrasts with the stable synapse and has different functional consequences.
Rapid migration during antigen recognition is observed in T-DC interactions in vitro early stages of T cell interaction with low dose agonist stimuli in vivo (Henrickson et al., 2008) and with low potency TCR stimuli (Skokos et al., 2007). There are at least two explanations for these mobile junctions or “kinapses”(Dustin, 2008). Certain chemokinetic signals, such as CCL21 signals, can compete with antigen stop signals (Bromley et al., 2000). The ability of T cells to migrate for some period followed by arrest may relate to signaling thresholds or time dependent down-regulation of CCR7. This gives the T cells flexibility in looking at different amounts of antigen on DCs-a few DCs with high amounts of MHC-peptide can stop T cells whereas many DCs with few antigen can sustain signaling until the T cells resets its sensitivity and can arrest (Henrickson et al., 2008). Weaker MHC-peptide never overcome the chemokinetic signals and continually migrate in DC networks (Skokos et al., 2007). T cells encountering these weaker ligands cannot arrest in the steady state and only integrate signals through kinapses. This mode of signal integration is sufficient to induce an alternative mode of tolerance induction when the antigen is presented on many DCs through scavenger receptor DEC-205. The failure of some weaker self-antigens to stop T cells may contribute the failure of tolerance induction and the development of autoimmuity (Zehn and Bevan, 2006). In autoimmunity the combination of strong innate signals and weak TCR signals can lead to robust responses, although there 