Autotaxin loss accelerates intestinal inflammation by suppressing TLR4-mediated immune responses.
ENPP2
ectonucleotide pyrophosphatase/phosphodiesterase family member 2
inflammatory bowel diseases
lipid raft
toll-like receptor 4
Journal
EMBO reports
ISSN: 1469-3178
Titre abrégé: EMBO Rep
Pays: England
ID NLM: 100963049
Informations de publication
Date de publication:
05 10 2020
05 10 2020
Historique:
received:
23
09
2019
revised:
20
07
2020
accepted:
10
08
2020
pubmed:
3
9
2020
medline:
28
4
2021
entrez:
3
9
2020
Statut:
ppublish
Résumé
Autotaxin (ATX) converts lysophosphatidylcholine and sphingosyl-phosphorylcholine into lysophosphatidic acid and sphingosine 1-phosphate, respectively. Despite the pivotal function of ATX in lipid metabolism, mechanisms by which ATX regulates immune and inflammatory disorders remain elusive. Here, using myeloid cell lineage-restricted Atx knockout mice, we show that Atx deficiency disrupts membrane microdomains and lipid rafts, resulting in the inhibition of Toll-like receptor 4 (TLR4) complex formation and the suppression of adaptor recruitment, thereby inhibiting TLR4-mediated responses in macrophages. Accordingly, TLR4-induced innate immune functions, including phagocytosis and iNOS expression, are attenuated in Atx-deficient macrophages. Consequently, Atx
Identifiants
pubmed: 32875703
doi: 10.15252/embr.201949332
pmc: PMC7534615
doi:
Substances chimiques
Tlr4 protein, mouse
0
Toll-Like Receptor 4
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e49332Subventions
Organisme : NIDDK NIH HHS
ID : K01 DK079015
Pays : United States
Organisme : National Research Foundation of Korea
ID : 2019R1A2C1010536
Informations de copyright
© 2020 The Authors.
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