Mengshol JA, Golden-Mason L, Castelblanco N, Im KA, Dillon SM, Wilson CC, and Rosen HR. (2009) Impaired plasmacytoid dendritic cell maturation and differential chemotaxis in chronic hepatitis C virus: associations with antiviral treatment outcomes. Gut 58:964-973.
Chronic hepatitis C (HCV) infection may be contributed to dendritic cell (DC) defects. DC are efficient antigen presenters and activators of antigen specific T cells and adaptive immunity. These cells may help determine the response of T cell stimulation to PEG-interferon and ribavirin therapy for HCV, but if the DC are defective, the claim was that there was a poor T cell response to HCV infection. In this study, matured DC defects and chemotaxis are used to compare therapeutic responders to non-responders. Samples of DC from 64 HCV-infected patients was analyzed 2 weeks before and 24 weeks after therapy. Flow cytometry was used to determine the amount of DCs and quantify chemokine receptor expression and an in vitro assay was used to measure chemotaxis. Results show that levels of CXCR3 and CXCR4 on DCs were higher compared to controls and decreased therapies. Pretreatment subjects of DCs were lower in HCV patients in comparison to the controls. Markers CD40 and CD83 were higher in DCs of patients infected with HCV compared to the controls. Chemotaxic of DCs to CXCL12 and CXCL10 showed failed antiviral responses. In conclusion, DC defects do occur in HCV patients, but successful antiviral therapy have normalized functional abnormalities.
Virology Spring 2011 