TITLE

Paradoxes and Pitfalls of Interleukin-33 in Atherosclerosis

AUTHOR(S)
Kunes, Pavel; Holubcova, Zdenka; Kolackova, Martina; Krejsek, Jan
PUB. DATE
January 2012
SOURCE
Open Clinical Chemistry Journal;2012, Vol. 5, p13
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
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 response 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.
ACCESSION #
80161517

 

Share

Read the Article

Courtesy of THE LIBRARY OF VIRGINIA

Sorry, but this item is not currently available from your library.

Try another library?
Sign out of this library

Other Topics