Therapeutic effect of omega-3 fatty acids on T cell-mediated autoimmune diseases.
Animals
Arthritis, Experimental
/ chemically induced
Disease Models, Animal
Encephalomyelitis, Autoimmune, Experimental
/ chemically induced
Fatty Acids, Omega-3
/ therapeutic use
I-kappa B Kinase
/ metabolism
Lymphocyte Activation
MAP Kinase Kinase Kinases
/ metabolism
NF-kappa B
/ metabolism
Rats
Rats, Sprague-Dawley
Receptors, G-Protein-Coupled
/ metabolism
Signal Transduction
T-Lymphocytes
/ immunology
Terpenes
GPR120
T cell
autoimmune disease
ω-3 fatty acids
Journal
Microbiology and immunology
ISSN: 1348-0421
Titre abrégé: Microbiol Immunol
Pays: Australia
ID NLM: 7703966
Informations de publication
Date de publication:
Aug 2020
Aug 2020
Historique:
received:
09
08
2019
revised:
22
04
2020
accepted:
05
05
2020
pubmed:
14
5
2020
medline:
16
4
2021
entrez:
14
5
2020
Statut:
ppublish
Résumé
The present study was to demonstrate that the G protein coupled receptors serve as targets for the treatment of autoimmune disease such as rheumatoid arthritis and multiple sclerosis. Rats received pristane at the base of the tail. Affected joints were counted daily. The T cell mediated autoimmune diseases such as pristine-induced arthritis (PIA) and autoimmune encephalomyelitis (EAE) in a rat model were profoundly ameliorated by treatment with the specific G protein couple receptors 120 (GPR120) stimuli omega-3 fatty acids (ω-3 FAs). Our study further revealed that the activation of GPR120 by ω-3 FAs can result in a decrease of phosphorylated transforming growth factor-β activated kinase 1 (TAK1), and further inhibit the downstream IKKβ/I-κB pathway and the terminal NF-κB activation which serves as a mediator of T cell activation. ω-3 Fatty acids exhibited an inhibitory effect on TAK1 by enhancing the association of β-arrestin2 and TAK1 binding protein 1 (TAB1), thus the disassociation of TAB1 from the TAB1/TAK1 complex renders a limited effect on β-arrestin2 signaling as an innate immunity regulation. GPR120 is a functional receptor of ω-3 fatty acids in T cell-mediated autoimmune disease compared with its effect on innate immunity.
Identifiants
pubmed: 32401403
doi: 10.1111/1348-0421.12800
doi:
Substances chimiques
Fatty Acids, Omega-3
0
NF-kappa B
0
Receptors, G-Protein-Coupled
0
Terpenes
0
pristane
26HZV48DT1
I-kappa B Kinase
EC 2.7.11.10
MAP Kinase Kinase Kinases
EC 2.7.11.25
MAP kinase kinase kinase 7
EC 2.7.11.25
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
563-569Informations de copyright
© 2020 The Societies and John Wiley & Sons Australia, Ltd.
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