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Letter
Co-stimulatory molecule CD80 expression may correlate with anti-HCV treatment outcome
  1. A Sacchi1,
  2. C Agrati1,2,
  3. G D'Offizi3,
  4. Chrysoula Vlassi3,
  5. F Martini1
  1. 1Laboratory of Cellular Immunology, National Institute for Infectious Diseases ‘Lazzaro Spallanzani’, Rome, Italy
  2. 2Laboratory of Virology, National Institute for Infectious Diseases ‘Lazzaro Spallanzani’, Rome, Italy
  3. 3Clinical Department, National Institute for Infectious Diseases ‘Lazzaro Spallanzani’, Rome, Italy
  1. Correspondence to Dr Alessandra Sacchi, Laboratory of Cellular Immunology, National Institute for Infectious Diseases ‘Lazzaro Spallanzani’, Via Portuense 292, Rome 00149, Italy; alessandra.sacchi{at}inmi.it

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It was estimated that up to 70% of hepatitis C virus (HCV)-infected subjects became chronically infected, and these patients have an increased risk of developing cirrhosis and hepatocellular carcinoma.1 The standard treatment for HCV-infected patients is pegylated interferon α (IFNα) in combination with ribavirin; however, data on the correlation between treatment outcome and the activation state of components of the immune system are missing. A very interesting paper by Mengshol et al was published in Gut regarding the effect of anti-HCV treatment on the activation state of circulating dendritic cells (DCs).2 The authors showed that levels of CXCR3 and CXCR4 on plasmacytoid DC (pDCs) were higher at baseline compared with controls, and decreased with treatment. Pretreatment levels of the co-stimulatory marker CD40 and the maturation marker CD83 were higher in pDCs of patients chronically infected with HCV compared with healthy controls; moreover, levels of both markers dropped significantly with treatment in the sustained virological responder (SVR) group only. Finally, baseline pDCs chemotaxis to CXCL12 …

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Footnotes

  • Competing interests None.

  • Patient consent Obtained.

  • Ethics approval This study was conducted with the approval of the INMI Lazzaro Spallanzani.

  • Provenance and peer review Not commissioned; externally peer reviewed.