Ghent University Academic Bibliography

Advanced

Inflammasome-dependent cytokines at the crossroads of health and autoinflammatory disease

Hanne Van Gorp UGent, Nina Van Opdenbosch and Mohamed Lamkanfi UGent (2018) COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY.
abstract
As key regulators of both innate and adaptive immunity, it is unsurprising that the activity of interleukin (IL)-1 cytokine family members is tightly controlled by decoy receptors, antagonists, and a variety of other mechanisms. Additionally, inflammasome-mediated proteolytic maturation is a prominent and distinguishing feature of two important members of this cytokine family, IL-1β and IL-18, because their full-length gene products are biologically inert. Although vital in antimicrobial host defense, deregulated inflammasome signaling is linked with a growing number of autoimmune and autoinflammatory diseases. Here, we focus on introducing the diverse inflammasome types and discussing their causal roles in periodic fever syndromes. Therapies targeting IL-1 or IL-18 show great efficacy in some of these autoinflammatory diseases, although further understanding of the molecular mechanisms leading to unregulated production of these key cytokines is required to benefit more patients.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (review)
publication status
in press
subject
journal title
COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY
Cold Spring Harbor Perspect. Biol.
ISSN
1943-0264
DOI
10.1101/cshperspect.a028563
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
8564408
handle
http://hdl.handle.net/1854/LU-8564408
date created
2018-06-06 12:26:21
date last changed
2018-06-14 11:39:46
@article{8564408,
  abstract     = {As key regulators of both innate and adaptive immunity, it is unsurprising that the activity of interleukin (IL)-1 cytokine family members is tightly controlled by decoy receptors, antagonists, and a variety of other mechanisms. Additionally, inflammasome-mediated proteolytic maturation is a prominent and distinguishing feature of two important members of this cytokine family, IL-1\ensuremath{\beta} and IL-18, because their full-length gene products are biologically inert. Although vital in antimicrobial host defense, deregulated inflammasome signaling is linked with a growing number of autoimmune and autoinflammatory diseases. Here, we focus on introducing the diverse inflammasome types and discussing their causal roles in periodic fever syndromes. Therapies targeting IL-1 or IL-18 show great efficacy in some of these autoinflammatory diseases, although further understanding of the molecular mechanisms leading to unregulated production of these key cytokines is required to benefit more patients.},
  author       = {Van Gorp, Hanne and Van Opdenbosch, Nina and Lamkanfi, Mohamed},
  issn         = {1943-0264},
  journal      = {COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY},
  language     = {eng},
  title        = {Inflammasome-dependent cytokines at the crossroads of health and autoinflammatory disease},
  url          = {http://dx.doi.org/10.1101/cshperspect.a028563},
  year         = {2018},
}

Chicago
Van Gorp, Hanne, Nina Van Opdenbosch, and Mohamed Lamkanfi. 2018. “Inflammasome-dependent Cytokines at the Crossroads of Health and Autoinflammatory Disease.” Cold Spring Harbor Perspectives in Biology.
APA
Van Gorp, H., Van Opdenbosch, N., & Lamkanfi, M. (2018). Inflammasome-dependent cytokines at the crossroads of health and autoinflammatory disease. COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY.
Vancouver
1.
Van Gorp H, Van Opdenbosch N, Lamkanfi M. Inflammasome-dependent cytokines at the crossroads of health and autoinflammatory disease. COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY. 2018;
MLA
Van Gorp, Hanne, Nina Van Opdenbosch, and Mohamed Lamkanfi. “Inflammasome-dependent Cytokines at the Crossroads of Health and Autoinflammatory Disease.” COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY (2018): n. pag. Print.