Are Anti–Oxidized Low-Density Lipoprotein Antibodies Pathogenic or Protective?

Shoenfeld, Yehuda; Wu, Ruihua; Dearing, Linda; Matsuura, Eiji

doi:10.1161/01.cir.0000143225.07377.ea

Cited by 133 publications

(119 citation statements)

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“…In addition to T cells, autoantibodies may also play a role in the acceleration of atherosclerosis. Autoantibodies to modified LDL are common in humans and increased levels of IgG antibodies to modified LDL have been suggested to be proatherogenic, whereas IgM antibodies to modified LDL may be anti-atherogenic [6]. Increased levels of IgG antibodies to modified LDL have been demonstrated in patients with vasculitis when compared with healthy controls [93,94].…”

Section: Cd28mentioning

confidence: 99%

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Translational Mini-Review Series on Immunology of Vascular Disease: Accelerated atherosclerosis in vasculitis

Tervaert

2009

Clinical and Experimental Immunology

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SummaryPremature atherosclerosis has been observed during the course of different systemic inflammatory diseases such as rheumatoid arthritis and sytemic lupus erythematosus. Remarkably, relatively few studies have been published on the occurrence of accelerated atherosclerosis in patients with vasculitis. In giant cell arteritis (GCA), mortality because of ischaemic heart disease is not increased. In addition, intima media thickness (IMT) is lower in patients with GCA than in age-matched controls. In contrast, IMT is increased significantly in Takayasu arteritis, another form of large vessel vasculitis occurring in younger patients. In Takayasu arteritis and in Kawasaki disease, a form of medium-sized vessel vasculitis, accelerated atherosclerosis has been well documented. In small vessel vasculitis because of anti-neutrophil cytoplasmic autoantibodies-associated vasculitis, cardiovascular diseases are a major cause of mortality. IMT measurements reveal conflicting results. During active disease these patients experience acceleration of the atherosclerotic process. However, when inflammation is controlled, these patients have atherosclerotic development as in healthy subjects. Several risk factors, such as diabetes and hypertension, are present more often in patients with vasculitis compared with healthy controls. In addition, steroids may be pro-atherogenic. Most importantly, many patients have impaired renal function, persistent proteinuria and increased levels of C-reactive protein, well-known risk factors for acceleration of atherosclerosis. Enhanced oxidation processes, persistently activated T cells and reduced numbers of regulatory T cells are among the many pathophysiological factors that play a role during acceleration of atherogenesis. Finally, autoantibodies that may be relevant for acceleration of atherosclerosis are found frequently in elevated titres in patients with vasculitis. Because patients have an increased risk for cardiovascular events, vasculitis should be treated with as much care as possible. In addition, treatment should be considered with angiotensin-converting-enzyme inhibitors and/or angiotensin receptor-1 blockers, statins and acetylsalicyl acid. Finally, classical risk factors for cardiovascular disease should be monitored and treated as much as possible.

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Section: Cd28mentioning

confidence: 99%

“…Regulatory T cells (Tregs), however, suppress this proinflammatory response [4,5]. Also, humoral immune responses may be either harmful or protective, and it has been postulated that some antibodies may result in acceleration of the atherosclerotic process, whereas other antibodies inhibit atherosclerosis [6].…”

Section: Introductionmentioning

confidence: 99%

Translational Mini-Review Series on Immunology of Vascular Disease: Accelerated atherosclerosis in vasculitis

Tervaert

2009

Clinical and Experimental Immunology

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“…One is a protective antibody that is induced by active immunization and is able to clear oxLDL cholesterol from the circulation, whereas the other types of antibody are pathogenic and play a role in the formation of foam cells. This could be due to the heterogeneous nature of these antibodies, which differ both in Ig subclass and in their epitope specificity and affinity (46).…”

Section: Protective Antibodies In Autoimmune Diseasesmentioning

confidence: 99%

Protective autoantibodies: Role in homeostasis, clinical importance, and therapeutic potential

Shoenfeld¹,

Toubi²

2005

Arthritis & Rheumatism

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“…It was also suggested that LDL modified by glycation, as it may occur in diabetic patients, may be more susceptible to oxidation ( Jenkins et al, 2004). Oxidatively modified LDL (oxLDL) that are strongly atherogenic may induce the immune response associated with enhanced production of specific autoantibodies against oxLDL (oLAb) (Steinerová et al, 2001;Shoenfeld et al, 2004). In the present study, the oLAb titers, the mean values of which were within the reference range set by Pincemail et al (2000) for the method used in our study, appeared to be independent of the degree of obesity and HOMA-IR estimated insulin resistance but, as could be predicted, they were correlated with serum LDL-C and the LDL-C/HDL-C ratio.…”

Section: Discussionmentioning

confidence: 99%