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Role of the 2B4 Receptor in CD8+ T-Cell-Dependent Immune Control of Epstein-Barr Virus Infection in Mice With Reconstituted Human Immune System Components

Chijioke, Obinna ; Marcenaro, Emanuela ; Moretta, Alessandro ; Capaul, Riccarda ; Münz, Christian

In: The Journal of Infectious Diseases, 2015, vol. 212, no. 5, p. 803-807

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    Titre
    • Role of the 2B4 Receptor in CD8+ T-Cell-Dependent Immune Control of Epstein-Barr Virus Infection in Mice With Reconstituted Human Immune System Components
    Auteur
    • Chijioke, Obinna. Viral Immunobiology, Institute of Experimental Immunology
    • Marcenaro, Emanuela. Deparment of Experimental Medicine
    • Moretta, Alessandro. Deparment of Experimental Medicine
    • Capaul, Riccarda. Institute of Medical Virology, University of Zurich, Switzerland
    • Münz, Christian. Viral Immunobiology, Institute of Experimental Immunology
    Type de document
    • Postprint
    Langue
    • Anglais
    Publié dans
    • The Journal of Infectious Diseases, 2015, vol. 212, no. 5, p. 803-807. Oxford University Press
    Autre version électronique
    Identifiant OAI-PMH
    • oai:doc.rero.ch:299181
    Summary
    Patients with X-linked lymphoproliferative (XLP) disease due to deficiency in the adaptor molecule signaling lymphocytic activation molecule-associated protein (SAP) are highly susceptible to one specific viral pathogen, the Epstein-Barr virus (EBV). This susceptibility might result from impaired CD8+ T-cell and natural killer cell responses to EBV infection in these patients. We demonstrate that antibody blocking of the SAP-dependent 2B4 receptor is sufficient to induce XLP-like aggravation of EBV disease in mice with reconstituted human immune system components. CD8+ T cells require 2B4 for EBV-specific immune control, because 2B4 blockade after CD8+ T-cell depletion did not further aggravate symptoms of EBV infection