| Literature DB >> 15639652 |
Hans J J van der Vliet1, Johan W Molling, B Mary E von Blomberg, Wendy Kölgen, Anita G Stam, Tanja D de Gruijl, Chris J Mulder, Harry L A Janssen, Nobusuke Nishi, Alfons J M van den Eertwegh, Rik J Scheper, Carin J M van Nieuwkerk.
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 alpha-galactosylceramide (alpha-GalCer, KRN7000). Previous studies have indicated that alpha-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 Valpha24+Vbeta11+ 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 Valpha24+Vbeta11+ 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 Valpha24+Vbeta11+ NKT cell ligand alpha-GalCer in HCV-infected patients are present.Entities:
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Year: 2005 PMID： 15639652 DOI： 10.1016/j.clim.2004.10.001
Source DB: PubMed Journal: Clin Immunol ISSN： 1521-6616 Impact factor: 3.969