BACKGROUND/AIMS: To investigate whether dendritic cell changes are associated with the efficacy of interferon-alpha treatment we longitudinally analyzed circulating dendritic cells in children chronically infected with hepatitis B virus (HBV) undergoing interferon-alpha treatment. METHODS: Thirty-one children with chronic hepatitis B (CHB) received interferon-alpha antiviral treatment for 52 weeks. Myeloid and plasmacytoid dendritic cell (pDCs) frequency and function were analyzed at weeks 0, 2, 12, 24, 36 and 52 in 22 CHB patients. RESULTS: All patients exhibited an initially rapid decrease of circulating pDC numbers and CpG-induced endogenous interferon-alpha production within 2 weeks of interferon-alpha treatment. Subsequently, all responders displayed a continuous increase of both pDC numbers and function peaking around week 12. These responses were consequently accompanied by viral clearance, hepatitis B e antigen seroconversion, and the improvement of circulating myeloid dendritic cells and type 1T helper cytokine levels. However, non-responders lacked these sequential responses compared with responders. CONCLUSIONS: pDCs may actively correlate with interferon-alpha therapy-induced viral clearance in pediatric patients with CHB. The recovery of blood pDC number and function may represent a prognostic marker for favourable response to interferon-alpha treatment in chronic hepatitis B.
BACKGROUND/AIMS: To investigate whether dendritic cell changes are associated with the efficacy of interferon-alpha treatment we longitudinally analyzed circulating dendritic cells in children chronically infected with hepatitis B virus (HBV) undergoing interferon-alpha treatment. METHODS: Thirty-one children with chronic hepatitis B (CHB) received interferon-alpha antiviral treatment for 52 weeks. Myeloid and plasmacytoid dendritic cell (pDCs) frequency and function were analyzed at weeks 0, 2, 12, 24, 36 and 52 in 22 CHB patients. RESULTS: All patients exhibited an initially rapid decrease of circulating pDC numbers and CpG-induced endogenous interferon-alpha production within 2 weeks of interferon-alpha treatment. Subsequently, all responders displayed a continuous increase of both pDC numbers and function peaking around week 12. These responses were consequently accompanied by viral clearance, hepatitis B e antigen seroconversion, and the improvement of circulating myeloid dendritic cells and type 1T helper cytokine levels. However, non-responders lacked these sequential responses compared with responders. CONCLUSIONS: pDCs may actively correlate with interferon-alpha therapy-induced viral clearance in pediatric patients with CHB. The recovery of blood pDC number and function may represent a prognostic marker for favourable response to interferon-alpha treatment in chronic hepatitis B.