Type I IFN-dependent FcγRIV signaling in murine monocytes promotes lethal anaphylaxis during viral infections - PubMed
6 days ago
- #Viral Infection
- #Monocytes
- #Anaphylaxis
- Type I IFN-dependent FcγRIV signaling in murine monocytes promotes lethal anaphylaxis during viral infections.
- Anaphylaxis is exacerbated during viral infections, driven by FcγRIV (homolog of human FcγRIIIa).
- Inflammatory monocytes are identified as the main drivers of lethal anaphylaxis in infected animals.
- Viral infection upregulates FcγRIV on inflammatory monocytes, absent in type I IFN receptor-deficient mice.
- Increased CD16-expressing classical monocytes observed in acute COVID-19 patients, replicated in murine SARS-CoV-2 infection.
- FcγRIV crosslinking during infection promotes platelet-activating factor production, key to mortality, in an IFN-I-dependent manner.
- Viral infection heightens monocyte sensitivity to Fcγ receptor engagement, making them major effectors of IgG-mediated hypersensitivity.
- Fc receptor pathway modulation suggested for investigation in conditions with heightened IFN-I responses, like systemic lupus erythematosus.