Necroptosis directly induces the release of full-length biologically active IL-33 in vitro and in an inflammatory disease model.
Animals
Apoptosis
/ drug effects
Aspergillus fumigatus
/ chemistry
Asthma
/ chemically induced
Basophils
/ drug effects
Cell Line
Complex Mixtures
/ administration & dosage
Disease Models, Animal
Eosinophils
/ drug effects
Female
Fibroblasts
/ drug effects
Gene Expression Regulation
Humans
Immunity, Innate
/ drug effects
Interleukin-33
/ genetics
Keratinocytes
/ drug effects
Mice
Mice, Inbred C57BL
Mice, Transgenic
Necrosis
/ genetics
Primary Cell Culture
Protein Kinase Inhibitors
/ pharmacology
Protein Kinases
/ genetics
Receptor-Interacting Protein Serine-Threonine Kinases
/ genetics
Signal Transduction
DAMP
MLKL
IL-33
cell death
necroptosis
Journal
The FEBS journal
ISSN: 1742-4658
Titre abrégé: FEBS J
Pays: England
ID NLM: 101229646
Informations de publication
Date de publication:
02 2019
02 2019
Historique:
received:
11
09
2018
revised:
10
11
2018
accepted:
18
12
2018
pubmed:
24
12
2018
medline:
9
8
2019
entrez:
22
12
2018
Statut:
ppublish
Résumé
Interleukin-33 (IL-33) is a pro-inflammatory cytokine that plays a significant role in inflammatory diseases by activating immune cells to induce type 2 immune responses upon its release. Although IL-33 is known to be released during tissue damage, its exact release mechanism is not yet fully understood. Previously, we have shown that cleaved IL-33 can be detected in the plasma and epithelium of Ripk1
Substances chimiques
Complex Mixtures
0
Il33 protein, mouse
0
Interleukin-33
0
Protein Kinase Inhibitors
0
MLKL protein, mouse
EC 2.7.-
Protein Kinases
EC 2.7.-
Receptor-Interacting Protein Serine-Threonine Kinases
EC 2.7.11.1
Ripk3 protein, mouse
EC 2.7.11.1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Pagination
507-522Subventions
Organisme : NIH HHS
ID : 5RO1HL124209
Pays : United States
Informations de copyright
© 2018 Federation of European Biochemical Societies.