Regulatory activity of polyunsaturated fatty acids in T-cell signaling.
Regulatory activity of polyunsaturated fatty acids in T-cell signaling.
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DOI：
10.1016/j.plipres.2010.01.002
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发表时间：
2010-07
影响因子：
13.6
通讯作者：
Chapkin, Robert S.
中科院分区：
文献类型：
--
作者：
Kim, Wooki;Khan, Naim A.;McMurray, David N.;Prior, Ian A.;Wang, Naisyin;Chapkin, Robert S.
n-3 多不饱和脂肪酸 (PUFA) 被认为是真正的免疫抑制剂，并且似乎对某些免疫介导的疾病发挥有益作用。除了促进辅助性 T 细胞 1 (Th1) 细胞向辅助性 T 细胞 2 (Th2) 效应 T 细胞分化外，n-3 PUFA 还可以通过诱导 Th1 细胞凋亡来发挥抗炎作用。就作用机制而言，影响范围从膜受体的调节到通过扰动许多第二信使级联的基因转录。在这篇综述中，我们将讨论在 T 细胞激活的早期和晚期事件中激活的抗炎 n-3 PUFA 的假定靶标。研究表明，这些脂肪酸会改变免疫突触处的质膜微组织（脂筏），T 细胞和抗原呈递细胞 (APC) 在此部位形成物理接触，以启动抗原启动的 T 细胞信号传导。此外，n-3 PUFA 还可调节二酰基甘油的产生以及蛋白激酶 C (PKC) 不同亚型、丝裂原激活蛋白激酶 (MAPK) 的激活、钙信号传导以及转录因子的核转位/激活。将批判性地介绍研究膜脂筏假说的不同方法的优点和局限性，以及 n-3 PUFA 对脂筏影响的明显矛盾。
n-3 polyunsaturated fatty acids (PUFA) are considered to be authentic immunosuppressors and appear to exert beneficial effects with respect to certain immune-mediated diseases. In addition to promoting T-helper 1 (Th1) cell to T-helper 2 (Th2) cell effector T-cell differentiation, n-3 PUFA may also exert anti-inflammatory actions by inducing apoptosis in Th1 cells. With respect to mechanisms of action, effects range from the modulation of membrane receptors to gene transcription via perturbation of a number of second messenger cascades. In this review, the putative targets of anti-inflammatory n-3 PUFA, activated during early and late events of T-cell activation will be discussed. Studies have demonstrated that these fatty acids alter plasma membrane micro-organization (lipid rafts) at the immunological synapse, the site where T-cells and antigen presenting cells (APC) form a physical contact for antigen initiated T-cell signaling. In addition, the production of diacylglycerol and the activation of different isoforms of protein kinase C (PKC), mitogen activated protein kinase (MAPK), calcium signaling, and nuclear translocation/activation of transcriptional factors, can be modulated by n-3 PUFA. Advantages and limitations of diverse methodologies to study the membrane lipid raft hypothesis, as well as apparent contradictions regarding the effect of n-3 PUFA on lipid rafts will be critically presented.
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