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ImmuneCited

Therapeutic effect of omega-3 fatty acids on T cell-mediated autoimmune diseases.

Liu Ouyang, Yang Dan, Wenbin Hua, Zengwu Shao, Deyu Duan
Other Microbiology and immunology 2020 8 цитирований
PubMed DOI
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Study Design

Тип исследования
Other
Популяция
None
Вмешательство
Therapeutic effect of omega-3 fatty acids on T cell-mediated autoimmune diseases. None
Препарат сравнения
None
Первичный исход
None
Направление эффекта
Positive
Риск систематической ошибки
Unclear

Abstract

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.

Кратко

GPR120 is a functional receptor of ω-3 FAs in the T cell-mediated autoimmune disease compared to its effect on the innate immunity, which 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-κBs activation which serves as a mediator of T cell activation.

Used In Evidence Reviews

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