Figure 2
Figure 2. Exposure of pDCs to HCVcc particles triggers the same activation signals as the crosslinking of DCIR and BDCA-2 regulatory receptors. Populations of magnetic bead-sorted pDCs were stimulated and followed by analysis of phosphorylation of Akt and Erk1/2 kinases by flow cytometry. Kinetics of phosphorylation of Akt and Erk1/2 in pDCs exposed to synthetic agonists CpG-A or R848, to HCV-infected Huh7.5 cells (Huh-HCV), or SGR-transfected Huh7.5 cells (Huh-SGR), to mock-infected Huh7.5 cells (Huh), to crosslinking with anti-DCIR or anti–BDCA-2 antibodies, to HCV particles (MOIHCV = 100), or to the mixtures of HCV particles with HCV-infected Huh7.5 cells (Huh-HCV + HCV particles). Data are mean ± SEM of 3-6 independent experiments with pDCs from different donors.

Exposure of pDCs to HCVcc particles triggers the same activation signals as the crosslinking of DCIR and BDCA-2 regulatory receptors. Populations of magnetic bead-sorted pDCs were stimulated and followed by analysis of phosphorylation of Akt and Erk1/2 kinases by flow cytometry. Kinetics of phosphorylation of Akt and Erk1/2 in pDCs exposed to synthetic agonists CpG-A or R848, to HCV-infected Huh7.5 cells (Huh-HCV), or SGR-transfected Huh7.5 cells (Huh-SGR), to mock-infected Huh7.5 cells (Huh), to crosslinking with anti-DCIR or anti–BDCA-2 antibodies, to HCV particles (MOIHCV = 100), or to the mixtures of HCV particles with HCV-infected Huh7.5 cells (Huh-HCV + HCV particles). Data are mean ± SEM of 3-6 independent experiments with pDCs from different donors.

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