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.

中文翻译：

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ω-3脂肪酸对T细胞介导的自身免疫性疾病的治疗作用。

本研究表明，G蛋白偶联受体可作为自身免疫性疾病（如类风湿性关节炎和多发性硬化症）的治疗靶标。大鼠在尾巴的底部接受了p烷。每天对患处进行计数。通过用特定的G蛋白偶联受体120（GPR120）刺激的ω-3脂肪酸（ω-）来治疗，可显着改善大鼠模型中T细胞介导的自身免疫性疾病，例如原始性关节炎（PIA）和自身免疫性脑脊髓炎（EAE）。 3个FA）。我们的研究进一步表明，ω-3FAs激活GPR120可导致磷酸化转化生长因子-β活化激酶1（TAK1）的减少，并进一步抑制下游IKKβ/I-κB途径和末端NF-κB。激活充当T细胞激活的介体。ω-3脂肪酸通过增强β-arrestin2与TAK1结合蛋白1（TAB1）的结合对TAK1表现出抑制作用，因此TAB1与TAB1 / TAK1复合物的解离对β-arrestin2信号传导的作用有限。天生的免疫调节。与它对先天免疫的影响相比，GPR120在T细胞介导的自身免疫性疾病中是ω-3脂肪酸的功能性受体。