Measles virus (MV) nucleoprotein binds to a novel cell surface receptor distinct from Fc[gamma]RII via its C-terminal domain : role in MV-induced immunosuppression

Laine David, Trescol-Biémont Marie-Claude, Longhi Sonia, Libeau Geneviève, Marie Julien C., Vidalain Pierre-Olivier, Azocar Olga, Diallo Adama, Canard Bruno, Rabourdin-Combe Chantal, Valentin Hélène. 2003. Measles virus (MV) nucleoprotein binds to a novel cell surface receptor distinct from Fc[gamma]RII via its C-terminal domain : role in MV-induced immunosuppression. Journal of Virology, 77 (21) : pp. 11332-11346.

Journal article ; Article de revue à facteur d'impact
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Liste HCERES des revues (en SHS) : oui

Thème(s) HCERES des revues (en SHS) : Psychologie-éthologie-ergonomie

Abstract : During acute measles virus (MV) infection, an efficient immune response occurs, followed by a transient but profound immunosuppression. MV nucleoprotein (MV-N) has been reported to induce both cellular and humoral immune responses and paradoxically to account for immunosuppression. Thus far, this latter activity has been attributed to MV-N binding to human and murine Fc[gamma]RII. Here, we show that apoptosis of MV-infected human thymic epithelial cells (TEC) allows the release of MV-N in the extracellular compartment. This extracellular N is then able to bind either to MV-infected or uninfected TEC. We show that recombinant MV-N specifically binds to a membrane protein receptor, different from Fc[gamma]RII, highly expressed on the cell surface of TEC. This new receptor is referred to as nucleoprotein receptor (NR). In addition, different Ns from other MV-related morbilliviruses can also bind to Fc[gamma]RII and/or NR. We show that the region of MV-N responsible for binding to NR maps to the C-terminal fragment (NTAlL). Binding of MV-N to NR on TEC triggers sustained calcium influx and inhibits spontaneous cell proliferation by arresting cells in the G0and G1 phases of the cell cycle. Finally, MV-N binds to both constitutively expressed NR on a large spectrum of cells from different species and to human activated T cells, leading to suppression of their proliferation. These results provide evidence that MV-N, after release in the extracellular compartment, binds to NR and thereby plays a role in MV-induced immunosuppression. (Résumé d'auteur)

Mots-clés Agrovoc : Morbillivirus, Réponse immunitaire, Biologie moléculaire, Cycle cellulaire, Nucléoprotéine

Mots-clés complémentaires : Rougeole

Classification Agris : L50 - Animal physiology and biochemistry

Auteurs et affiliations

  • Laine David, INSERM (FRA)
  • Trescol-Biémont Marie-Claude, INSERM (FRA)
  • Longhi Sonia, CNRS (FRA)
  • Libeau Geneviève, CIRAD-EMVT-SANTE ANIMALE (FRA)
  • Marie Julien C., INSERM (FRA)
  • Vidalain Pierre-Olivier, INSERM (FRA)
  • Azocar Olga, INSERM (FRA)
  • Canard Bruno, CNRS (FRA)
  • Rabourdin-Combe Chantal, INSERM (FRA)
  • Valentin Hélène, INSERM (FRA)

Autres liens de la publication

  • Document en bibliothèque
  • Localisation du document : BA_BR2645 [(Bibliothèque de Baillarguet)] ; BA_BR2662 [(Bibliothèque de Baillarguet)]

Source : Cirad - Agritrop (

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