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Bacterial coinfection restrains antiviral CD8 T-cell response via LPS-induced inhibitory NK cells

Author

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  • Tobias Straub

    (Medical Center – University of Freiburg, Faculty of Medicine, University of Freiburg)

  • Marina A. Freudenberg

    (University of Freiburg
    Medical Center – University of Freiburg, Faculty of Medicine, University of Freiburg)

  • Ulrike Schleicher

    (Friedrich Alexander-Universität (FAU) Erlangen-Nürnberg
    Medical Immunology Campus Erlangen, FAU Erlangen-Nürnberg)

  • Christian Bogdan

    (Friedrich Alexander-Universität (FAU) Erlangen-Nürnberg
    Medical Immunology Campus Erlangen, FAU Erlangen-Nürnberg)

  • Georg Gasteiger

    (University of Wuerzburg
    University of Freiburg Medical Center)

  • Hanspeter Pircher

    (Medical Center – University of Freiburg, Faculty of Medicine, University of Freiburg)

Abstract

Infection of specific pathogen-free mice with lymphocytic choriomeningitis virus (LCMV) is a widely used model to study antiviral T-cell immunity. Infections in the real world, however, are often accompanied by coinfections with unrelated pathogens. Here we show that in mice, systemic coinfection with E. coli suppresses the LCMV-specific cytotoxic T-lymphocyte (CTL) response and virus elimination in a NK cell- and TLR2/4-dependent manner. Soluble TLR4 ligand LPS also induces NK cell-mediated negative CTL regulation during LCMV infection. NK cells in LPS-treated mice suppress clonal expansion of LCMV-specific CTLs by a NKG2D- or NCR1-independent but perforin-dependent mechanism. These results suggest a TLR4-mediated immunoregulatory role of NK cells during viral-bacterial coinfections.

Suggested Citation

  • Tobias Straub & Marina A. Freudenberg & Ulrike Schleicher & Christian Bogdan & Georg Gasteiger & Hanspeter Pircher, 2018. "Bacterial coinfection restrains antiviral CD8 T-cell response via LPS-induced inhibitory NK cells," Nature Communications, Nature, vol. 9(1), pages 1-9, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-06609-z
    DOI: 10.1038/s41467-018-06609-z
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