Mechanisms of Disease: atherosclerosis in autoimmune diseases

Abstract

Atherosclerosis is a pathologic process affecting blood vessels, which leads to the development of cardiovascular disease. The immune system is involved in atherogenesis and in the pathogenesis of atherosclerosis. Several autoimmune rheumatic conditions, including rheumatoid arthritis, systemic lupus erythematosus and antiphospholipid syndrome, are characterized by enhanced atherosclerosis and consequently higher cardiovascular morbidity and mortality rates. Enhanced atherosclerosis, in these diseases, can manifest as overt cardiovascular diseases, but could be detected at an earlier stage by identification of abnormal endothelial function and arterial intima-media thickening. Both classical and nonclassical risk factors are presumed to contribute to atherosclerosis progression in rheumatic diseases. As atherosclerosis can be considered to be an immune-mediated process, several experimental strategies exist for its immunomodulation, including induction of immune tolerance. In this article, we briefly review the contribution of autoimmune elements, such as autoreactive lymphocytes and autoantibodies to atherosclerosis and discuss the nature of atherosclerosis in autoimmune rheumatic diseases.

The role of resistin as a regulator of inflammation: Implications for various human pathologies

“…Patients with systemic rheumatic diseases generally have an increased prevalence of atherosclerosis [107]. Very recently, a decline in serum levels of resistin after TNF-α blocking therapy has been shown; it is evident that this therapy, in addition to reducing joint inflammation, can concomitantly improve the cardiovascular prognosis in inflammatory disorders [108,109].…”

CD40-activated B cells from patients with systemic lupus erythematosus can be modulated by therapeutic immunoglobulins in vitro

“…In many autoimmune disorders, IVIg treatment results in the suppression of pathological autoimmune antibodies in patient serum for prolonged periods of time (Branch et al 2001;Kaveri et al 1991). Since IVIg contains anti-idiotypic antibodies capable of binding to these pathological autoantibodies, many authors have postulated that IVIg can directly and specifically modulate autoreactive B cells (Kazatchkine et al 1994;Seite et al 2008;Sherer and Shoenfeld 2006b;Shoenfeld and Katz 2005;Vani et al 2008) and by doing so restore immune homeostasis in patients with autoimmune diseases. The use of IVIg in the treatment of SLE can result in partial to complete remission in patients with various manifestations of SLE [reviewed in (ZandmanGoddard et al 2005)]; however, its use is often restricted to SLE patients who did not respond to standard treatment (Sherer and Shoenfeld 2006a).…”

Antigen Presentation After Stroke

“…However, considerable evidence supports a relationship between systemic inflammation and poor outcome in patients with stroke and in experimental stroke models. Many components of the immune system are involved in the pathological processes underlying the development of atherosclerosis and its ischemic complications [103]. In patients, stroke can produce an inflammatory response known as systemic inflammatory response syndrome, which is especially frequent in patients with severe stroke.…”