Skip to main content
. 2017 Nov 27;8:1633. doi: 10.3389/fimmu.2017.01633

Figure 2.

Figure 2

Impact of type I IFNs on protective (green) and detrimental (red) host responses in the immune-competent Mycobacterium tuberculosis-infected host. The current literature suggests that in the immune-competent host, type I IFNs suppress host-protective IFN-γ and IL-1α/β responses, as well as the recruitment of mycobacteria-restricting monocytes/macrophages. In contrast, type I IFN signaling can directly induce NO production, a contributor to effective antimycobacterial host defense. The evidence for the contributions of type I IFNs to host-protective interleukin-12 and TNF responses is currently ambiguous and may be determined by timing, dose, and source of the type I IFN response. Type I IFNs are a driver of IL-10, a cytokine that impairs antimycobacterial immune responses during all stages of infection. Type I IFN signatures in patients have been associated with neutrophils and studies in mouse models of heightened M. tuberculosis susceptibility suggest that type I IFN signaling facilitates infection of permissive neutrophils, which have been associated with damaging tissue pathology.