Author/Authors :
van der Vliet، نويسنده , , Hans J.J and Molling، نويسنده , , Johan W. and von Blomberg، نويسنده , , B. Mary E. and Kِlgen، نويسنده , , Wendy and Stam، نويسنده , , Anita G. and de Gruijl، نويسنده , , Tanja D. and Mulder، نويسنده , , Chris J. and Janssen، نويسنده , , Harry L.A. and Nishi، نويسنده , , Nobusuke and van den Eertwegh، نويسنده , , Alfons J.M. and Scheper، نويسنده , , Rik J.، نويسنده ,
Abstract :
CD1d-restricted natural killer T (NKT) cells are involved in the regulation of various immune responses, and have been shown to inhibit viral replication in animal hepatitis models when activated by the glycolipid α-galactosylceramide (α-GalCer, KRN7000). Previous studies have indicated that α-GalCer-induced activation of the immune system requires both CD1d expression by antigen-presenting cells as well as (normal) numbers of NKT cells. Discrepancies exist over circulating numbers of human invariant Vα24+Vβ11+ NKT cells during hepatitis C virus (HCV) infection. Here, by cross-sectional analysis and longitudinal analysis of patients undergoing effective combination antiviral therapy, we demonstrate that circulating Vα24+Vβ11+ NKT cell numbers are not decreased during active HCV infection. Importantly, as we also show that CD1d is expressed at comparable levels by peripheral blood monocytes and CD1c+ myeloid dendritic cells (DC) of healthy individuals and HCV-infected patients, these data indicate that all ingredients for evaluating the antiviral effects of the Vα24+Vβ11+ NKT cell ligand α-GalCer in HCV-infected patients are present.
