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A more recent version of this article appeared on December 30, 2005
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M509796200v1
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Papers In Press, published online ahead of print October 10, 2005
J. Biol. Chem, 10.1074/jbc.M509796200
Submitted on September 7, 2005
Revised on October 5, 2005
Accepted on October 10, 2005

The docosatriene protectin D1 is produced by TH2-skewing and promotes human T cell apoptosis via lipid-raft clustering

Amiram Ariel, Pin-Lan Li, Wei Wang, Wang-Xian Tang, Gabrielle Fredman, Song Hong, Katherine H. Gotlinger, and Charles N. Serhan

Center for Experimental Therapeutics and Reperfusion Injury, Brigham and Women's Hospital/Harvard Medical School, Boston, MA 02115

Corresponding Author: cnserhan{at}zeus.bwh.harvard.edu

Docosahexaenoic acid (DHA), a major omega -3 fatty acid in human brain, synapses, retina, and other neural tissues, displays beneficial actions in neuronal development, cancer, and inflammatory diseases by mechanisms that remain to be elucidated. In this study, we found, using lipid mediator-informatics employing LC-MS-MS, that 10,17S-docosatriene/neuroprotectin D1, now termed protectin D1 (PD1), is generated from DHA by T helper type 2 (TH2)-skewed peripheral blood mononuclear cells (PBMC) in a lipoxygenase-dependent manner. PD1 blocked T cell migration in vivo, inhibited TNFalpha and IFNgamma secretion, and promoted apoptosis mediated by raft clustering. These results demonstrate novel anti-inflammatory roles for PD1 in regulating events associated with inflammation and resolution.


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