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Measles virus nucleoprotein induces cell-proliferation arrest and apoptosis through NTAIL-NR and NCORE-FcgammaRIIB1

D Laine1, J M Bourhis2, S Longhi2

  • 1Laboratoire d'Immunobiologie Fondamentale et Clinique, INSERM U503 and UCBL1, IFR128 BioSciences Lyon-Gerland, 21 Avenue Tony Garnier, 69365 Lyon Cedex 07, France.

The Journal of General Virology
|May 26, 2005
PubMed

Insights

Measles virus nucleoprotein (MV-N) has two domains that suppress cell proliferation through distinct mechanisms. NTAIL arrests cell cycle, while NCORE triggers apoptosis via FcgammaRIIB1, offering potential therapeutic targets.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Measles virus (MV) nucleoprotein (N) is released extracellularly after infected cell death.
  • Extracellular MV-N interacts with cell surface receptors FcgammaRIIB and a nucleoprotein receptor (NR).

Purpose of the Study:

  • To investigate the distinct roles of MV-N domains (NCORE and NTAIL) and their interactions with FcgammaRIIB and NR in suppressing cell proliferation.
  • To elucidate the mechanisms underlying MV-N-mediated immunosuppression.

Main Methods:

  • Utilized a human melanoma cell line (HT144) engineered to express or lack FcgammaRIIB1.
  • Employed domain-specific MV-N proteins and deletion mutants to analyze receptor interactions and cellular responses.
  • Assessed cell cycle progression and apoptosis using flow cytometry and caspase activation assays.

Main Results:

  • NTAIL binding to NR primarily caused G0/G1 cell cycle arrest.
  • NCORE binding to FcgammaRIIB1 triggered caspase-3 activation and apoptosis, dependent on the receptor's intracellular tail.
  • The NTAIL region, specifically Box1 (aa 401-420), is crucial for NR binding and cell growth arrest.

Conclusions:

  • Distinct domains of MV-N mediate different immunosuppressive activities through specific receptor interactions.
  • MV-N's mechanisms of cell proliferation suppression and apoptosis induction provide insights into MV-induced immunosuppression.
  • MV-N domains represent potential therapeutic targets for modulating tumor cell proliferation and apoptosis.

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