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. Author manuscript; available in PMC: 2017 Sep 1.
Published in final edited form as: Curr Opin Rheumatol. 2016 Sep;28(5):468–476. doi: 10.1097/BOR.0000000000000307

Figure 1.

Figure 1

Potential pathways promoting atherosclerosis in SLE

Endothelial dysfunction (ED) may be induced by an imbalance of vascular damage (triggered by innate and adaptive immune stimuli) and impaired vascular repair induced by a dysfunction of endothelial progenitor cells (EPCs) induced by type I IFNs and metabolic dysfunction. Various proinflammatory pathways in the plaque may induce neutrophils to undergo NETosis and promote further inflammatory cell recruitment, induce endothelial cell death, enhance local type I IFN synthesis, oxidize lipoproteins and promote thrombosis. Type I IFNs and other stimuli may promote enhanced foam cell formation. Decrease in B Regulatory cells (BRegs) may promote loss of natural IgM, impaired apoptosis and increased IFNs at the level of the plaque. Platelet activation may lead to acute coronary syndromes.