The impact of macroautophagy on CD8+ T-cell-mediated antiviral immunity

Authors

  • Brieuc P. Perot,

    1. Unité d'immunobiologie des cellules dendritiques, Institut Pasteur, Paris, France
    2. Inserm U818, Paris, France
    3. Université Pierre et Marie Curie, Paris, France
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  • Molly A. Ingersoll,

    1. Unité d'immunobiologie des cellules dendritiques, Institut Pasteur, Paris, France
    2. Inserm U818, Paris, France
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  • Matthew L. Albert

    Corresponding author
    1. Inserm U818, Paris, France
    2. Universite Paris Descartes, Paris, France
    • Unité d'immunobiologie des cellules dendritiques, Institut Pasteur, Paris, France
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Correspondence to:

Matthew L. Albert

25 Rue du Docteur Roux

75724 Paris Cedex 15, France

Tel.: +33 1 45 68 80 71

Fax: +33 1 45 68 85 48

e-mail: albertm@pasteur.fr

Summary

Macroautophagy is a catabolic recycling pathway, which can be induced by various stress stimuli. Viruses are able to manipulate autophagy in the cells that they infect. The impact of autophagy on the innate immune response to viruses and its stimulatory role in antigen presentation to CD4+ T cells are well documented. Herein, we present the impact of autophagy on the activation of cytotoxic T lymphocyte (CTL)-mediated antiviral immune responses, which are required for the eradication or control of multiple viruses. We first discuss the general mechanisms by which viruses can either induce or block autophagy in cells. We then explore the cross-talk between autophagy and innate immune processes, which are both first line defenses against viruses; and constitute crucial steps for the initiation of potent adaptive immune responses. We describe the impact of autophagy on the presentation of viral peptide antigens on class I major histocompatibility complex (MHC I), a prerequisite for the priming of CTL responses. In sum, our review highlights the interplay between viruses and three integrated host response pathways – autophagy, innate and adaptive immunity – providing a framework for future mechanistic and pathogenesis-based research.

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