Gabriele Campi

TL;DR: It is proposed that T CR signaling is sustained by stabilized microclusters and is terminated in the cSMAC, a structure from which TCR are sorted for degradation, and a role for F-actin in TCR signaling beyond microcluster formation is revealed.

TL;DR: T cell receptor (TCR) microclusters form within seconds of T cell contact with supported planar bilayers containing intercellular adhesion molecule-1 and agonist major histocompatibility complex (MHC)-peptide complexes, and elevation of cytoplasmic Ca2+ is observed within seconds after the first detectable micro-clusters as mentioned in this paper.

TL;DR: In vitro and in silico experiments are used to determine that the immunological synapse acts as a type of adaptive controller that both boosts T cell receptor triggering and attenuates strong signals.

TL;DR: Analysis of the resulting alternatively patterned synapses revealed a causal relation between the radial position of T cell receptors (TCRs) and signaling activity, with prolonged signaling from TCR microclusters that had been mechanically trapped in the peripheral regions of the synapse.

TL;DR: LFA-1 acts through PLD2 to reshape the pattern of Ras activation downstream of the TCR, which increases DAG levels at the plasma membrane by stimulating phospholipase D (PLD) and phosphatidic acid phosphatase (PAP).