Platelet-derived major histocompatibility complex class I coating on attenuates natural killer cell lethality.

The evasive tactics of pose a major challenge in combating and eradicating syphilis. Natural killer (NK) cells mediate important effector functions in the control of pathogenic infection, preferentially eliminating targets with low or no expression of major histocompatibility complex (MHC) class I. To clarify mechanisms in evading NK-mediated immunosurveillance, experiments were performed to explore the cross-talk relations among , NK cells, and platelets. adhered to, activated, and promoted particle secretion of platelets. After preincubation with , platelets expressed and secreted high levels of MHC class I, subsequently transferring them to the surface of , potentially inducing an immune phenotype characterized by the "pseudo-expression" of MHC class I on the surface of (hereafter referred to a "pseudo-expression" of MHC class I). The mRNA assay showed that platelet-preincubated group exhibited a significantly higher copy number of transcript than the group. The survival rate of mirrored that of mRNA, indicating that preincubation of with platelets attenuated NK cell lethality. Platelets pseudo-expressed the MHC class I ligand on the surface, facilitating binding to killer cell immunoglobulin-like receptors with two immunoglobulin domains and long cytoplasmic tail 3 (KIR2DL3) on NK cells and initiating dephosphorylation of Vav1 and phosphorylation of Crk, ultimately attenuating NK cell lethality. Our findings elucidate the mechanism by which platelets transfer MHC class I to the surface to evade NK cell immune clearance.