Fig. 3.

Schematic depicting interaction of cellular subsets in the presence of IFN-I. IFN-α influences the activity of surrounding innate and adaptive immune cells. It remains unknown what initially triggers the cascade of IFN production; however, it has been suggested that the generation of DNA/RNA via cell death pathways including apoptosis, necrosis, and NETosis (with subsequent ROS generation) plays a role. Exposure to these self-antigens increases the risk of developing autoantibodies, which form immune complexes that have potential to interact with IFN-producing cells to enhance further IFN-I production. Monocytes develop an inflammatory phenotype and activated cDCs promote activation of CD4+ and CD8+ T cell subsets. These T cells themselves upon exposure to IFN-I can further enhance B cell activation and mediation of cell death, respectively. cDCs, conventional dendritic cells; IFN-𝛂, interferon-𝛂; NET, neutrophil extracellular traps; ROS, reactive oxygen species