title: Actual position of interleukin(IL)-33 in atherosclerosis and heart failure: Great Expectations or En attendant Godot?
abstract: Atherosclerosis has been recognized as an inflammatory/autoimmune disease. The long-standing low-grade inflammation which fuels its development is primarily focused on the components of the vessel wall. Originally, inflammation in atherogenesis was supposed to be driven by the pro-inflammatory Th1 cellular and cytokine immune response. On the basis of accumulating evidence, this view has been re-evaluated to include the Th17/Th1 axis which is shared by most diseases of sterile inflammation. The anti-inflammatory Th2 cellular and cytokine immune response is initiated concomitantly with the former two, the latter dampening their harmful reactions which culminate in full-blown atherosclerosis. Interleukin-33, a novel member of the IL-1 cytokine superfamily, was suggested to take part in the anti-atherogenic response by mediating the Th1-to-Th2 switch of the immune reactions. However, IL-33 is a multifaceted mediator with both pro- and anti-inflammatory activities, also called a "dual factor" or a "Janus face" interleukin. IL-33 occurs both in an extracellular (cytokine-like) and in a nuclear-bound (transcription factor-like) form, each of them performing distinct activities of their own. This review article presents the latest data relevant to IL-33's role in atherosclerosis and cardiac diseases as perceived by a cardiologist and a cardiac surgeon.
authors.affiliation: Department of Cardiac Surgery, Charles University in Prague, Faculty of Medicine and University Hospital in Hradec Kralove, Czech Republic.
authors.forename: P
authors.initials: P
authors.lastname: Kunes
authors.affiliation: Department of Cardiac Surgery, Charles University in Prague, Faculty of Medicine and University Hospital in Hradec Kralove, Czech Republic.
authors.forename: J
authors.initials: J
authors.lastname: Mandak
authors.affiliation: Department of Cardiac Surgery, Charles University in Prague, Faculty of Medicine and University Hospital in Hradec Kralove, Czech Republic.
authors.forename: Z
authors.initials: Z
authors.lastname: Holubcova
authors.affiliation: Department of Clinical Immunology and Allergology, Charles University in Prague, Faculty of Medicine and University Hospital in Hradec Kralove, Czech Republic.
authors.forename: M
authors.initials: M
authors.lastname: Kolackova
authors.affiliation: Department of Clinical Immunology and Allergology, Charles University in Prague, Faculty of Medicine and University Hospital in Hradec Kralove, Czech Republic jan.krejsek@fnhk.cz.
authors.forename: J
authors.initials: J
authors.lastname: Krejsek
mesh_terms: D050197:Atherosclerosis / Q000276:immunology* / Q000473:pathology; D006333:Heart Failure / Q000276:immunology* / Q000473:pathology; D006801:Humans; D000067596:Interleukin-33 / Q000276:immunology*; D018417:Th1 Cells / Q000276:immunology* / Q000473:pathology; D058504:Th17 Cells / Q000276:immunology* / Q000473:pathology; D018418:Th2 Cells / Q000276:immunology* / Q000473:pathology
chemical_list: C506536:IL33 protein, human; D000067596:Interleukin-33
keywords: IL-33; Th1; Th17; Th2; atherosclerosis; cytokine; inflammation; transcription factor