re needed for sensitive recognition of rare MHC-peptide ligands. The links between TCR signaling and polarity networks include Cdc42 and PKC-ζ. Activation of Cdc42 has been extensively studied in T cells due to interest in immunodeficiencies such as Wiscott-Alrdrich Syndrome. PKC-ζ can be activated in the Par3-Par6 complex by activation of Cdc42, but it is not clear what it means that PKC-ζ is concentrated in the distal pole complex, the part of the T cell farthest from the synapse (Chang et al., 2007). The polarity networks control the positioning of actin, microtubules and intermediate filament and spindles. The dynamic F-actin networks and myosin II seem important at early stages of signaling complex assembly. The actin-myosin system is critical for multiple stages in TCR triggering and sustained signaling. It will be exciting in the future to determine in more detail how the context of TCR signaling allows this process to shape differentiation in parallel with powerful innate signals.
I thank Kaushik Choudhuri and David Fooksman for valuable discussions. Due to length constraints not all relevant literature could be cited and I apologize in advance regarding omissions. This work was supported by NIH grants AI43542and the PN2 EY016586, a Nanomedicine Development Center.