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HBcAg did not modulate pDC function (Fig. 5).
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In addition to the direct effect of HBV on pDC, HBV seems also able to indirectly influence pDC function by interfering with monocyte-pDC interaction.
Recently, BDCA-2 was proposed as receptor involved in pDC-HBsAg interaction leading to active inhibition of pDC function [14].
Moreover, HBV interfered with TLR9-induced pDC function, resulting in dose-dependent inhibition of cytokine production and pDC maturation.
HBV not only directly interfered with pDC function, but also indirectly by interfering with monocyte-pDC interaction.
Serum ALT levels inversely correlated with pDC function, which indicates that also other regulatory mechanisms than the virus itself may influence pDC function.
Also HBeAg diminished pDC function to a certain extent, but via another unknown mechanism.
In this study, we investigated the impact of HCV on pDC function.
HBV/HBsAg also diminished upregulation of co-stimulatory molecules, production of TNFα, IP-10 and IL-6 and pDC-induced NK cell function, whereas TLR7-induced pDC function was hardly affected.
HBeAg impaired pDC function to a much lesser extent and seemingly via another yet unknown intracellular signalling mechanism.
Supernatants derived from non-transfected HepG2 cells served as a control and did not influence pDC function (data not shown).
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com