Author/Authors :
Diego Piccioli، نويسنده , , Simona Tavarini، نويسنده , , Sandra Nuti، نويسنده , , Piero Colombatto، نويسنده , , Maurizia Brunetto، نويسنده , , Ferruccio Bonino، نويسنده , , Pietro Ciccorossi، نويسنده , , Francesca Zorat، نويسنده , , Gabriele Pozzato، نويسنده , , Consuelo Comar، نويسنده , , Sergio Abrignani، نويسنده , , Andreas Wack، نويسنده ,
Abstract :
Background/Aims
Dendritic cells (DCs) play a key role in immune responses through antigen presentation and cytokine secretion. Hepatitis C virus (HCV) is able to escape elimination by the immune system and often establishes a chronic infection. To investigate whether DC dysfunction is involved in this process, we have studied monoycte-derived DCs (Mo-DCs) and plasmacytoid DCs (pDCs), which produce large amounts of IFN-α, from chronic HCV patients and healthy donors.
Methods
We have assessed TNF-α and IFN-α production by pDCs using intracellular staining after total PBMCs stimulation with unmethylated CG dinucleotides (CpGs). The induction of allogeneic T cell proliferation by immature Mo-DCs was measured using the MLR assay. The up-regulation of maturation markers and the production of TNF-α in response to LPS were analyzed using flow cytometry and ELISA, respectively.
Results
We have detected comparable frequencies of pDCs producing TNF-α and IFN-α in both chronic HCV patients and healthy donors and we have found that immature Mo-DCs from both patients and donors similarly induce allogeneic T cell proliferation and mature and secrete TNF-α in response to LPS.
Conclusions
Our results demonstrate that both pDC and Mo-DCs are not impaired in HCV infected patients.
Keywords :
TNF-a , IFN-a , dendritic cell , HCV , maturation