Reciprocal regulation of human natural killer cells and macrophages associated with distinct immune synapses.

摘要: Natural killer (NK) cells directly lyse tumor or viral-infected but also an important role for NK cell cytotoxicity in regulating the extent of immune responses is emerging. Here, we show that autologous human macrophages activated proliferation and cytokine secretion, increased expression activating receptors, primed against susceptible target cells. Ligation 2B4, not NKp30 (known to be DC-mediated activation), critical this macrophage-mediated activation. Reciprocally, however, regulated macrophage activity by killing stimulated high doses LPS. Cytolysis was triggered NKG2D recognition stress-inducible class I major histocompatibility complex (MHC)-like ligands on macrophages: LPS induced transcription surface ULBP1, ULBP2, ULBP3 constitutively transcribed MICA. Thus, these data suggest a new function eliminating overstimulated macrophages. Additionally, interactions define, first time, 2 distinct synapses: lytic nonlytic. Triggering cytolysis, specifically associated with synaptic accumulation F-actin while were killed when ICAM-1 accumulated around central cluster NKG2D/DAP10.