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Dtsch Med Wochenschr. 2013 Sep;138(37):1839-44. doi: 10.1055/s-0033-1349426. Epub 2013 Sep 4.

[Chronic inflammation and atherosclerosis].

[Article in German]

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Institut für Prophylaxe und Epidemiologie der Kreislaufkrankheiten (IPEK), Klinikum der Universität München, Ludwig-Maximilians-Universität München und Deutsches Zentrum für Herz-Kreislaufforschung (DZHK), Partnerstandort Munich Heart Alliance.


The increasing gain of knowledge regarding the mechanistic details of the pathogenesis of chronic inflammatory diseases e. g. of rheumatic origin, chronic viral infections and atherosclerosis have revealed in conjunction with detailed insights in acute inflammation interesting similarities and differences. Cytokines such as IL-1 and tumour necrosis factor-α are proximal components of inflammatory cascades of systemic mediators activating the endothelium which leads to an endothelial dysfunction and moreover alter the balance within lymphocytic subpopulations containing distinct arsenals of secretory mediators such as interferons, interleukins and chemokines. Proinflammatory lymphocyte subtypes are TH1 und TH17 cells whereas Treg and TH2 cells are anti-inflammatory opponents. Since several years, interleukin-1- and TNF-antagonists have expanded the spectrum of drugs against rheumatic diseases and are currently studied in the setting of cardiovascular prevention with positive results on surrogate parameters. On the other hand efforts are undertaken to test the hypothesis if the pleiotropic effects of statins may have a positive influence on rheumatoid arthritis.

[Indexed for MEDLINE]

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