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.
We evaluated the role of TLR2 and TLR4 signaling in the induction of both PD and atherosclerosis in TLR2<sup>-/-</sup> and TLR4<sup>-/-</sup> mice to polymicrobial infection with periodontal pathogens Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Fusobacterium nucleatum.