Multiple target cells can be quickly killed by cytotoxic T cells( CTLs ), necessitating a controlled transition from recognition to detachment from each target cell. Stinchcombe et al. published Science. Discover that when the T cell receptor( TCR ) is activated, membrane specialization within the immune cell synapse occurs. Activated TCRs are then released into ectosomes that are endocytosed by the target cell, stopping the signaling of the CTL and enabling serial killing. The authors discovered that CD3 was primarily found in ectosomes that protruded from the edge of the central supramolecular activation cluster or were detached from CTL membranes by imaging the immune cell synapse between target cells and CDTLs. As ectosomes protruded from the CTL, the tight membrane contacts between them and the target cells were lost, resulting in a region of localized cell separation between the two. Membrane-associated CD3 decreased as the size of the cells increased. Increased ectocytosis and increased CTL detachment from target cells were the results of stronger TCR signal strength. In clathrin-adorned structures, budding ectosomes were carried up into dying target cells. As a result, activated TCR is shed by ectocytosis at the immune cell synapse rather than being endocytosed and subsequently degraded.Access the preview of subscription content here by going to your institution.options for access
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