Inflammasomes contributing to inflammation in arthritis.

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State: Public
Version: Author's accepted manuscript
License: Not specified
Serval ID
serval:BIB_DE14124731A8
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Title
Inflammasomes contributing to inflammation in arthritis.
Journal
Immunological reviews
Author(s)
Spel L., Martinon F.
ISSN
1600-065X (Electronic)
ISSN-L
0105-2896
Publication state
Published
Issued date
03/2020
Peer-reviewed
Oui
Volume
294
Number
1
Pages
48-62
Language
english
Notes
Publication types: Journal Article ; Review
Publication Status: ppublish
Abstract
Inflammasomes are intracellular multiprotein signaling platforms that initiate inflammatory responses in response to pathogens and cellular damage. Active inflammasomes induce the enzymatic activity of caspase-1, resulting in the induction of inflammatory cell death, pyroptosis, and the maturation and secretion of inflammatory cytokines IL-1β and IL-18. Inflammasomes are activated in many inflammatory diseases, including autoinflammatory disorders and arthritis, and inflammasome-specific therapies are under development for the treatment of inflammatory conditions. In this review, we outline the different inflammasome platforms and recent findings contributing to our knowledge about inflammasome biology in health and disease. In particular, we discuss the role of the inflammasome in the pathogenesis of arthritic diseases, including rheumatoid arthritis, gout, ankylosing spondylitis, and juvenile idiopathic arthritis, and the potential of newly developed therapies that specifically target the inflammasome or its products for the treatment of inflammatory diseases.
Keywords
CARD8, NLRP3, arthritis, gout, inflammasome, innate immunity
Pubmed
Web of science
Open Access
Yes
Funding(s)
Swiss National Science Foundation / Projects / 310030173152
Create date
23/01/2020 16:48
Last modification date
29/04/2020 6:20
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