Moreover, our data offer an explanation for the comparable effects of IFNα or IFNγ priming on TLR4-induced activation in vascular and immune cells, with important implications in atherosclerosis.
ART counteracts the effect of IFNα to inhibit MIF production by blocking STAT1 phosphorylation and thus may have therapeutic potential for SLE-associated atherosclerosis.
Patients with systemic lupus erythematosus are genetically predisposed to enhanced production of the type-I interferon IFN-α and are also at elevated risk of developing atherosclerosis compared with healthy subjects.
The aim of this study was to determine whether IFNα is involved in the development of atherosclerosis in patients with SLE by promoting lipid uptake and macrophage-derived foam cell formation, which is a crucial step in early atherosclerosis.
Chlamydophila pneumoniae infection of the vascular wall as well as activation of the transcription factor IFN regulatory factor (IRF)3 have been linked to development of chronic vascular lesions and atherosclerosis.
These observations suggest that one mechanism by which IFN-g promotes atherosclerosis may involve affecting expression of cholesterol 27-hydroxylase, a cholesterol homeostatic protein.