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. Author manuscript; available in PMC: 2019 Aug 16.
Published in final edited form as: Mol Cell. 2018 Aug 16;71(4):637–648.e5. doi: 10.1016/j.molcel.2018.07.010

Figure 6. CBL represses antiviral responses during viral infection.

Figure 6.

(A) BMMs infected with Sendai virus (SeV) for 24h, and the relative number of virions in the supernatant were quantified by RT-qPCR; Mean ± SEM displayed. Phase-contrast image (10x) at 24h post-infection. Scale bars = 100 microns.

(B) Infection with HSV-1 for 24h, analyzed as above. t-tests were used for statistical analysis.

(C) BMMs were infected with lpqN mutant Mtb for 6h and analyzed by Western blot.

(D) Model of balance between antiviral and antibacterial cell-intrinsic immune response pathways mediated by CBL. Host macrophages tailor responses to distinct kinds of pathogens at the earliest stages of infection by activating cell-intrinsic immune pathways tailored to the threat, e.g. virus or bacterium. These programs appear to be mutually antagonistic, as activation of antiviral pathways comes at the cost of antibacterial immunity during Mtb infection. Our work indicates that CBL functions to influence this balance by inhibiting viral responses and promoting antibacterial immunity.