Affiliation:
1. Unidad de Investigación, Hospital Universitario Reina Sofia, Instituto de Investigacion Biomédica de Córdoba (IMIBIC), E-14004 Córdoba, Spain
2. Hospital Virgen de la Victoria, Fundación IMABIS, E-29010 Málaga, Spain
3. Lupus Research Unit, St Thomas Hospital, London SE1 7EH, UK
Abstract
Systemic lupus erythematosus (SLE), a chronic multisystem autoimmune disease with a broad range of clinical manifestations, is associated with accelerated atherosclerosis (AT) and increased risk of cardiovascular complications. Relevant factors directly influencing the development of AT comprise immune complex generation, complement activation, and changes in the production and activity of a complex network of cytokines, including type I and II interferons, B lymphocyte stimulator (BLyS), TNFα, IL-6, IL-17 and migration macrophage inhibitor (MIF). Autoantibodies, also responsible for cytokine expression and activation, play a supplementary key role in the development of AT. Genomic and proteomic studies have contributed to the discovery of genes and proteins involved in AT, including some that may be suitable to be used as biomarkers. All that data has allowed the development of new drugs, most of them evaluated in clinical trials: inhibitors of IFN and TNFα, B cell directed therapies, synthetic oligodeoxynucleotides, intravenous immunoglobulin, or statins. The focus of the present paper is to summarize recent evidence showing the role of cytokines in the development of AT in SLE and the rationale, and safety concerns, in the use of combined therapy to prevent AT and cardiovascular disease.
Subject
Health, Toxicology and Mutagenesis,Genetics,Molecular Biology,Molecular Medicine,General Medicine,Biotechnology
Cited by
34 articles.
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