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human NK cells. KIRs that were found at low abundance assembled into smaller clusters than those formed by KIRs that were more highly abundant, and at low abundance there was a greater proportion of KIRs in clusters. Upon receptor triggering, a structured interface called an immune synapse assembles, which facilitates signal integration and controls the NK cell response. Here, low-abundance receptors exhibited less phosphorylation of downstream hosphatase SHP-1 but more phosphorylation of adaptor protein Crk than did high-abundance receptors. In cells with greater KIR abundance, SHP-1 dephosphorylated Crk, which potentiated the NK cell spreading response during activation. Thus, genetic variation modulates both the abundance and nanoscale
organization of inhibitory KIRs. In other words, as well as the number of receptors at the cell surface varying with genotype, the way in which these receptors are organized in the membrane also varies. Essentially, a change in the average surface abundance of a protein at the cell surface is a coarse descriptor entwined with changes in local nanoscale clustering. Altogether, our data indicate that genetic diversity in inhibitory KIRs affects membrane-proximal signaling and surprisingly, the formation of activating immune synapses.
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- 1 Finished
1/09/16 → 30/09/22