Abstract
There is interest in developing new compounds to enhance the immune response to airway virus infections. CVT-E002 is a patented ginseng extract shown to decrease symptoms of virus infection in clinical trials. We hypothesized that the mechanism for this antiviral effect could be through modulation of dendritic cells leading to enhanced T-cell activation. Human monocyte-derived dendritic cells (moDC) exposed to CVT-E002 (or not) were co-cultured with autologous T cells, with or without virus (respiratory syncytial virus or parainfluenza virus). Effects of CVT-E002 on cell function were determined through flow cytometry, 5-bromo-2'-deoxyuridine (BrdU) incorporation and ELISA. moDC cultured with CVT-E002 or virus induced greater activation of T cells, as measured by CD25 expression and BrdU incorporation, compared with untreated moDC. Responding T cells were CD4+CD45RO+. Co-cultures of CVT-E002 treated moDC with T cells responded with increased release of Th1-type cytokines (interferon-gamma, tumour necrosis factor and interleukin-12). CVT-E002-treated moDC showed increased expression of CD83, CD80 and CD86. Lipopolysaccharide levels were not detected in CVT-E002 and antagonists for Toll-like receptor-4 did not inhibit CVT-E002-induced moDC maturation. CVT-E002 induced moDC maturation, which caused increased memory T-cell activation and Th1-type cytokine response.
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