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环氧化酶及其代谢产物对辅助性 T 细胞亚群的调节。

Regulation of T helper cell subsets by cyclooxygenases and their metabolites.

机构信息

Laboratory of Respiratory Biology, Division of Intramural Research, NIEHS/NIH, Research Triangle Park, NC 27709, USA.

出版信息

Prostaglandins Other Lipid Mediat. 2013 Jul-Aug;104-105:74-83. doi: 10.1016/j.prostaglandins.2012.11.002. Epub 2012 Nov 28.

DOI:10.1016/j.prostaglandins.2012.11.002
PMID:23201570
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3620713/
Abstract

Cyclooxygenases and their metabolites are important regulators of inflammatory responses and play critical roles in regulating the differentiation of T helper cell subsets in inflammatory diseases. In this review, we highlight new information on regulation of T helper cell subsets by cyclooxygenases and their metabolites. Prostanoids influence cytokine production by both antigen presenting cells and T cells to regulate the differentiation of naïve CD4(+) T cells to Th1, Th2 and Th17 cell phenotypes. Cyclooxygenases and PGE2 generally exacerbate Th2 and Th17 phenotypes, while suppressing Th1 differentiation. Thus, cycloxygenases may play a critical role in diseases that involve immune cell dysfunction. Targeting of cyclooxygenases and their eicosanoid products may represent a new approach for treatment of inflammatory diseases, tumors and autoimmune disorders.

摘要

环氧化酶及其代谢产物是炎症反应的重要调节因子,在调节炎症性疾病中 T 辅助细胞亚群的分化中起着关键作用。在这篇综述中,我们强调了环氧化酶及其代谢产物对 T 辅助细胞亚群调节的新信息。前列腺素既影响抗原呈递细胞又影响 T 细胞产生细胞因子,从而调节初始 CD4+T 细胞向 Th1、Th2 和 Th17 细胞表型的分化。环氧化酶和 PGE2 通常加重 Th2 和 Th17 表型,同时抑制 Th1 分化。因此,环氧化酶可能在涉及免疫细胞功能障碍的疾病中发挥关键作用。靶向环氧化酶及其类花生酸产物可能代表治疗炎症性疾病、肿瘤和自身免疫性疾病的新方法。

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本文引用的文献

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