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* Department of Biological Sciences, Kean University, Union, NJ 07083;
Department of Medicine, St. Joseph’s Regional Medical Center, Paterson, NJ 07503; and
Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA 19140
In contrast to the role of dendritic cells (DC) in immunity and tolerance, little is known about their possible role in the resolution of inflammatory processes. In addition to the reduction in the number of infiltrating immune cells, the elimination of effector T cells already present at the inflammatory site represents an essential step toward resolution. Recently, lipid mediators such as the omega-3 fatty acids eicosapentaenoic acid and docosahexaenoic acid and their metabolites, including resolvin E1 (RvE1), have been shown to accumulate in inflammatory foci during the resolution phase. RvE1 has been reported to reduce immune cell infiltration and proinflammatory cytokine production. In this study we report that DC exposed to RvE1, especially during differentiation, acquire the capacity to induce apoptosis of activated T cells through the induction and activity of indoleamine 2,3-dioxygenase. To our knowledge, this study is the first to report on an omega-3 fatty acid derivative inducing indoleamine 2,3-dioxygenase expression in DC. RvE1-exposed DC maintain an immature chemokine receptor expression pattern even following TLR stimulation, with high CCR5 and no CCR7 expression. This effect implies that DC exposed to RvE1 and pathogens remain at the inflammatory site, instead of migrating to lymph nodes, and induce apoptosis in effector T cells infiltrating the inflammatory site. To our knowledge, the DC described in this study represent a new functional DC subtype, whose essential function resides in the resolution of inflammation.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by Grant R01AI052306 from the National Institute of Allergy and Infectious Diseases, National Institutes of Health (to D.G.) and a grant from the Office of Research and Sponsored Programs of Kean University (to E.K.V.).
2 Address correspondence and reprint requests to Dr. Evros K. Vassiliou, Department of Biological Sciences, Science Building, Kean University, 1000 Morris Avenue, Union, NJ 07083. E-mail address: evassili{at}kean.edu
3 Abbreviations used in this paper: EPA, eicosapentaenoic acid; DHA, docosahexaenoic acid; COX, cyclooxygenase; DC, dendritic cell; PCCF, pigeon cytochrome c fragment; Treg, regulatory T cell; Tg, transgenic; IDO, indoleamine 2,3-dioxygenase; PI, propidium iodide; PMN, polymorphonuclear cell; RvE1, resolvin E1.
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