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  • Atherosclerosis is definitely considered as an inflammatory/immunopathological disease. The long-standing low-grade inflammation is focused on the components of the vessel wall. Initially, this inflammation was assumed to be driven by the pro-inflammatory Th1 cellular and cytokine immune responses. On the basis of accumulating knowledge, however, this view has been specified to include the Th17/Th1 axis which underlies most immunopathological diseases accompanied by sterile inflammation. On the other hand, an anti-inflammatory Th2 cellular and cytokine immune re-sponse attempts to dampen these unfavorable reactions which terminate in full-blown atherosclerosis. Interleukin-33, the 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. IL-33 presents both an extracellular (cytokine-like) and a nuclear-bound (transcription factor-like) form, each of them performing distinct activities of their own. This review article summarizes latest data relevant to IL-33's role in atherosclerosis, underscoring the paradoxes and pitfalls of laboratory findings and their extrapolation to live organisms including humans.
  • Atherosclerosis is definitely considered as an inflammatory/immunopathological disease. The long-standing low-grade inflammation is focused on the components of the vessel wall. Initially, this inflammation was assumed to be driven by the pro-inflammatory Th1 cellular and cytokine immune responses. On the basis of accumulating knowledge, however, this view has been specified to include the Th17/Th1 axis which underlies most immunopathological diseases accompanied by sterile inflammation. On the other hand, an anti-inflammatory Th2 cellular and cytokine immune re-sponse attempts to dampen these unfavorable reactions which terminate in full-blown atherosclerosis. Interleukin-33, the 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. IL-33 presents both an extracellular (cytokine-like) and a nuclear-bound (transcription factor-like) form, each of them performing distinct activities of their own. This review article summarizes latest data relevant to IL-33's role in atherosclerosis, underscoring the paradoxes and pitfalls of laboratory findings and their extrapolation to live organisms including humans. (en)
Title
  • Paradoxes and Pitfalls of Interleukin-33 in Atherosclerosis
  • Paradoxes and Pitfalls of Interleukin-33 in Atherosclerosis (en)
skos:prefLabel
  • Paradoxes and Pitfalls of Interleukin-33 in Atherosclerosis
  • Paradoxes and Pitfalls of Interleukin-33 in Atherosclerosis (en)
skos:notation
  • RIV/00179906:_____/12:10123801!RIV13-MZ0-00179906
http://linked.open...avai/predkladatel
http://linked.open...avai/riv/aktivita
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  • I
http://linked.open...iv/cisloPeriodika
  • 1
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  • 157743
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  • RIV/00179906:_____/12:10123801
http://linked.open...riv/jazykVysledku
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  • Th1-to-Th2 transition; gene transcription; lipid metabolism; inflammation; atherosclerosis; ST2 receptor; Interleukin-33 (en)
http://linked.open.../riv/klicoveSlovo
http://linked.open...odStatuVydavatele
  • NL - Nizozemsko
http://linked.open...ontrolniKodProRIV
  • [B28281975F30]
http://linked.open...i/riv/nazevZdroje
  • Open Clinical Chemistry Journal
http://linked.open...in/vavai/riv/obor
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  • 5
http://linked.open...iv/tvurceVysledku
  • Krejsek, Jan
  • Koláčková, Martina
  • Kuneš, Pavel
  • Holubcová, Zdeňka
issn
  • 1874-2416
number of pages
http://bibframe.org/vocab/doi
  • 10.2174/1874241601205010013
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