Immunosuppressive function of hepatitis B antigens in vitro: role of endoribonuclease V as one potential trans inactivator for cytokines in macrophages and human hepatoma cells

J Virol. 1990 May;64(5):1956-63. doi: 10.1128/JVI.64.5.1956-1963.1990.

Abstract

The mRNAs of transiently expressed cytokine genes contain AUUUA-rich sequences in the 3' untranslated regions. In order to examine whether the AU-specific endoribonuclease V (EC 3.1.27.8) described previously by us transinactivates those mRNA species, we introduced a 51-nucleotide ATTTA sequence from tumor necrosis factor into the 3' untranslated region of beta-globin gene. Transcripts of that construct, synthesized in vitro, were prone to endoribonuclease V digestion at those AU-rich sequences. Stimulation of human macrophages with lipopolysaccharide resulted in a shift of the association state of the enzyme from the nuclear matrix-associated to the free form. This shift was strongly prevented by the hepatitis B surface antigen (HBsAg) and more weakly by hepatitis B nucleocapsid antigen and hepatitis B antigen of the X region. HBsAg and, to a lesser extent, hepatitis B nucleocapsid antigen and hepatitis B antigen of the X region inhibited the release of alpha interferon, tumor necrosis factor alpha, and granulocyte-macrophage colony stimulating factor, while it had no effect on interleukin-1 production from stimulated macrophages. Using the human hepatoma cell line PLC/PRF/5, we provide further experimental evidence that endoribonuclease V acts in trans as a posttranscriptional inactivator for nuclear matrix-associated cytokine transcripts. These results suggest that those cytokine transcripts which contain reiterated (overlapping) AUUUA sequences are degraded by nuclear matrix-associated endoribonuclease V. This degradation was comparably high in cells incubated with HBsAg or cells which produced this antigen.

MeSH terms

  • Animals
  • Base Sequence
  • Biological Factors / genetics*
  • Carcinoma, Hepatocellular
  • Cattle
  • Cell Line
  • Cell Nucleus / metabolism
  • Cells, Cultured
  • Cytokines
  • Endoribonucleases / metabolism*
  • Gene Amplification
  • Gene Expression Regulation*
  • Globins / genetics
  • Hepatitis B Surface Antigens / immunology*
  • Humans
  • Immunosuppression Therapy*
  • Lipopolysaccharides / pharmacology
  • Liver Neoplasms
  • Macrophages / drug effects
  • Macrophages / immunology
  • Macrophages / metabolism*
  • Molecular Sequence Data
  • Nucleic Acid Hybridization
  • Oligonucleotide Probes
  • Plasmids
  • Substrate Specificity
  • Thymus Gland / enzymology
  • Tumor Cells, Cultured / metabolism*

Substances

  • Biological Factors
  • Cytokines
  • Hepatitis B Surface Antigens
  • Lipopolysaccharides
  • Oligonucleotide Probes
  • Globins
  • Endoribonucleases
  • ribonuclease V