Figure 3.

The effect of type-I IFNs during atherosclerosis development in different models. Atherosclerosis is driven by predisposing risk factors such as dysregulated lipids, pro-inflammatory stimuli, and cytokines. The development of the lesion is characterized by lipid trapping, leukocyte infiltration and activation, foam cell formation, fibrous cap, and extracellular lipid core formation. In unstable, complex plaques, fibrous cap thinning and necrosis take place, which lead to plaque rupture. The dots, from left to right, represent the effect on the corresponding event due to “type-I IFNs, IFNAR signaling blockade in mice,” “lupus-prone mice or type-I IFN treatment in mice,” “anti-type-I IFN/IFNAR treatment in human,” and “interferonopathy patients or type-I IFN treatment in human,” respectively. For each dot, the left hemisphere of the dot indicates in vitro or ex vivo data, while the right means in vivo studies.