Abstract

and reporter gene assays, respectively. Expression of cell surface markers (CD80, CD86, CD40, MHC-II) were assessed by FACS. Results: TLR3 induced stimulation of antiviral activities; IFN production and expression of interferon-stimulated genes in NPC were potently suppressed by pretreatment with IL-10 or TGF-b. This correlated with suppression of TLR3 receptor expression and inhibition of TLR-induced activation of NF-uB and IRF-3 in these cells. T cell activation induced by TLR3-stimulated NPC was suppressed by IL-10 and TGF-b which was associated with a downregulation of costimulatory cell surface molecules (CD80, CD86). Conclusions: HCV/TLR3-mediated innate and adaptive immune functions of non-parenchymal liver cells are potently controlled by IL-10 and TGF-b. This is of relevance for the regulation of the local immune responses against viral infections of the liver and the pathogenesis of HCV infection in particular.

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