Patients with systemic lupus erythematosus (SLE) have up to a 50-fold increased risk of developing atherosclerotic cardiovascular disease. Traditional CV risk factors seem to be less important predictors of CV events than the presence of active SLE. Indeed, immune dysregulation characteristic of lupus appears to play the dominant role in atherogenesis. While both SLE-specific and non-specific mechanisms have been proposed to play a prominent role in the induction of premature vascular damage in this disease, the exact etiology remains unclear. We have proposed that an imbalance between vascular damage and repair likely induced by Interferon-α and other type I Interferons could play a prominent role in the induction of accelerated atherosclerosis in SLE. Our group and others have recently elucidated the potential role that these cytokines play in the development and progression of premature atherosclerotic disease in SLE and, potentially, in other autoimmune diseases. We have recently described some of the pathways by which IFN-alpha has deleterious effects on angiogenesis in endothelial progenitor cells and circulating angiogenic cells. Strong evidence pointing to a deleterious role of type I IFNs in aberrant vasculogenesis and atherothrombosis has recently been described by our group. More recently, a novel role for aberrant neutrophils in the development of vascular damage and abnormal vascular repair in SLE has emerged. The recent description of a distinct subset of proinflammatory neutrophils isolated from lupus patients which induces vascular damage and synthesizes type I Interferons has shed new light into a potentially important cell subset implicated in endothelial damage.
Disclosure of Interest None Declared
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