[11][12] The initial interaction occurs between LFA-1 present in the p-SMAC of a T-cell, and non-specific adhesion molecules (such as ICAM-1 or ICAM-2) on a target cell.
These interactions activate large multi-molecular complexes (containing WAVE (Scar), HSP300, ABL2, SRA1, and NAP1 and others) to associate with Arp2/3, which directly promotes actin polymerization.
Even after receiving weak or short-lived signals, the MTOC polarizes towards the immunological synapse, but in that case the lytic granules are not trafficked and therefore the killing effect is missing or poor.
After initiation of the cell-cell contact, the lytic granules of NK cells move around the microtubules towards the centrosome, which also relocalizes towards the site of synapse.
SMIC then acts to prevent rearrangement of actin, block the recruitment of activatory receptors to the site of synapse and finally, promote detachment from the target cell.
[17] Immunological synapses were first discovered by Abraham Kupfer at the National Jewish Medical and Research Center in Denver.
Daniel M. Davis and Jack Strominger showed structured immune synapses for a different lymphocyte, the Natural Killer cell, and published this around the same time.
[20] Abraham Kupfer first presented his findings during a Keystone Symposia in 1995, when he showed three-dimensional images of immune cells interacting with one another.