Activation of STING requires its translocation from the endoplasmic reticulum (ER) through the Golgi to vesicles, but the mechanisms that control its localization have been unclear. The ER calcium sensor STIM1 acts as an ER-retention factor that anchors STING on the ER and limits STING signaling.

A new model proposes that an applied force allows the co-receptor CD8 and the kinase Lck to selectively stabilize TCR interactions with negatively selecting ligands, but not those with positively selecting ligands, during the negative selection of self-reactive thymocytes.

G protein coupled receptors (GPCRs) transmit a variety of signals, mostly by engaging G proteins, but G protein-independent signalling through arrestins has also been demonstrated. Based on recent experimental evidence, Gutkind and Kostenis argue that arrestins serve as important signal modulators instead of as independent signal transducers.

T cell activation is ‘digital’: exhaustive single-cell analysis shows that only the proportion of cells that cross the activation threshold is reduced when the affinity of the TCR for its ligand is reduced.