Rapid, label-free, volumetric, and automated assessment of the immunological synapse dynamics is demonstrated by combining optical diffraction tomography and deep-learning-based segmentation, providing a new option for immunological research.

Inhibition of the catalytic activity of the Zap70 kinase reveals that discrete TCR-regulated events control the remodelling of the actin cytoskeleton when the cytotoxic T cell interacts with its target.

Kinesin-4 KIF21B promotes rapid reorientation of the microtubule network during formation of immunological synapse in T cells by acting as a pausing and catastrophe-inducing factor that keeps microtubules short.

T cell receptor signaling is regulated by newly polymerized F-actin foci at the immunological synapse.

Modeling the dynamics of immunological synapses informs pharmacodynamics and treatment resistance to bispecific T cell engagers.

Upon activation of T cell receptors at the contact site, T cells were substantially stiffened at the cell body as well as at the lamellipodia, which is mediated by Ca²⁺.

HLA-B*35:01 molecules that are peptide-deficient are thermostable, bind CD8 with higher affinity than their peptide-filled versions, accumulate at immunological synapses and enhance antigen-specific CD8+ T cell immune responses.

TCR and CD40L microclusters are linked in synaptic ectosomes (extracellular vesicles) and released in the immunological synapse by helper T cells and induce dendritic cell maturation and cytokine production.

By restricting actin polymerization to the perimeter of the immune synapse and promoting depolymerization, calcium influx drives centripetal actin flow, which confines CRAC channels and the endoplasmic reticulum to the synapse center.

Sorting nexin 9, a membrane curvature inducing protein, creates a distinct environment within clusters of the co-receptor CD28 and thereby allows T cell activation to proceed to a successful outcome.