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Activated intrahepatic antigen-presenting cells inhibit hepatitis B virus replication in the liver of transgenic mice

Academic Article
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Overview

authors

  • Kimura, K.
  • Kakimi, K.
  • Wieland, Stefan
  • Guidotti, Luca
  • Chisari, Francis

publication date

  • 2002

journal

  • Journal of Immunology  Journal

abstract

  • In this study we evaluated the ability of activated intrahepatic APCs to inhibit hepatitis B virus (HBV) replication in transgenic mice. Intrahepatic APCs were activated by administration of an anti-CD40 agonistic mAb (alphaCD40). We showed that a single i.v. injection of alphaCD40 was sufficient to inhibit HBV replication noncytopathically by a process associated with the recruitment of dendritic cells, macrophages, T cells, and NK cells into the liver and the induction of inflammatory cytokines. The antiviral effect depended on the production of IL-12 and TNF-alpha by activated APCs; however, it was mediated primarily by IFN-gamma produced by NK cells, and possibly T cells, that were activated by IL-12. Collectively, these results suggest that activated APCs can directly produce antiviral cytokines (IL-12, TNF-alpha) and trigger the production of other cytokines (i.e., IFN-gamma) by other cells (e.g., NK cells and T cells) that do not express CD40. These results provide insight into a hitherto unsuspected antiviral function of intrahepatic APCs, and they suggest that therapeutic activation of APCs may represent a new strategy for the treatment of chronic HBV infection.

subject areas

  • Animals
  • Antibodies, Monoclonal
  • Antigen-Presenting Cells
  • Antigens, CD40
  • Antiviral Agents
  • Cell Movement
  • Hepatitis B virus
  • Inflammation
  • Injections, Intravenous
  • Interferon-gamma
  • Interleukin-12
  • Liver
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, Transgenic
  • T-Lymphocytes
  • Tumor Necrosis Factor-alpha
  • Virus Replication
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Identity

International Standard Serial Number (ISSN)

  • 0022-1767

PubMed ID

  • 12391236
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Additional Document Info

start page

  • 5188

end page

  • 5195

volume

  • 169

issue

  • 9

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