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

Tobias Straub, Marina A. Freudenberg, Ulrike Schleicher, Christian Bogdan, Georg Gasteiger and Hanspeter Pircher ()
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Tobias Straub: Medical Center – University of Freiburg, Faculty of Medicine, University of Freiburg
Marina A. Freudenberg: University of Freiburg
Ulrike Schleicher: Friedrich Alexander-Universität (FAU) Erlangen-Nürnberg
Christian Bogdan: Friedrich Alexander-Universität (FAU) Erlangen-Nürnberg
Georg Gasteiger: University of Wuerzburg
Hanspeter Pircher: Medical Center – University of Freiburg, Faculty of Medicine, University of Freiburg

Nature Communications, 2018, vol. 9, issue 1, 1-9

Abstract: 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.

Date: 2018
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DOI: 10.1038/s41467-018-06609-z

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