Type I Interferon Signaling Prevents IL-1β-Driven Lethal Systemic Hyperinflammation during Invasive Bacterial Infection of Soft Tissue.
Dagmar Stoiber contributed to a new study now published by Pawel Kovarik from the MFPL. Type I interferons (IFN-Is) are fundamental for antiviral immunity, but their role in bacterial infections is contradictory and incompletely described. The authors report that IFN-I signaling protects the host against invasive Streptococcus pyogenes infection by restricting inflammation-driven damage in distant tissues. Critical cellular effectors of IFN-I in vivo are LysM+ and CD11c+ myeloid cells, which exhibit suppression of Il1b transcription upon Ifnar1 engagement. These cells are also the major source of IFN-β, which is significantly induced by S. pyogenes 23S rRNA in an Irf5-dependent manner. This research establishes IL-1β and IFN-I levels as key homeostatic variables of protective, yet tuned, immune responses against severe invasive bacterial infection.
Congratulations to Dagmar Stoiber and her colleagues to this interesting report and fine success.