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Actual position of interleukin(IL)-33 in atherosclerosis and heart failure: Great Expectations or En attendant Godot
P. Kunes, J. Mandak, Z. Holubcova, M. Kolackova, J. Krejsek,
Jazyk angličtina Země Anglie, Velká Británie
Typ dokumentu časopisecké články, práce podpořená grantem, přehledy
NLK
ProQuest Central
od 1997-01-01 do 2015-11-30
SAGE Publications Journals
od 1999-01-01 do 2015-12-31
CINAHL Plus with Full Text (EBSCOhost)
od 1997-01-01 do 2016-05-31
Medline Complete (EBSCOhost)
od 1997-01-01 do 2016-05-31
Nursing & Allied Health Database (ProQuest)
od 1997-01-01 do 2015-11-30
Health & Medicine (ProQuest)
od 1997-01-01 do 2015-11-30
PubMed
25501624
DOI
10.1177/0267659114562269
Knihovny.cz E-zdroje
- MeSH
- ateroskleróza imunologie patologie MeSH
- buňky Th17 imunologie patologie MeSH
- interleukin 33 imunologie MeSH
- lidé MeSH
- srdeční selhání imunologie patologie MeSH
- Th1 buňky imunologie patologie MeSH
- Th2 buňky imunologie patologie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
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.
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