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Blood, 1 October 2005, Vol. 106, No. 7, pp. 2375-2381. Prepublished online as a Blood First Edition Paper on June 9, 2005; DOI 10.1182/blood-2005-03-0979. This Article Full Text (PDF) Supplemental Figures All Versions of this Article: 2005-03-0979v1 106/7/2375    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Braun, D. Articles by Albert, M. L Search for Related Content PubMed PubMed Citation Articles by Braun, D. Articles by Albert, M. L Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted March 10, 2005 Accepted May 12, 2005 A two step induction of indoleamine 2,3 dioxygenase (IDO) activity during dendritic cell maturation Deborah Braun, Randy S Longman, and Matthew L Albert* Institut Pasteur, Paris, France; Avenir 0201, INSERM, Paris, France * Corresponding author; email: albertm{at}pasteur.fr. Prostaglandins, a family of lipidic molecules released during inflammation, display immunomodulatory properties in several models. One use includes exposure of monocyte-derived dendritic cells (DCs) to a cocktail of cytokines that contains prostaglandin E2 (PGE2) for purposes of maturation-such cells are currently being used for cancer immunotherapy trials. Our analysis of the transcription profile of DCs matured in the presence of TNF and PGE2 revealed a strong up-regulation of indoleamine 2-3 dioxygenase (IDO), an enzyme involved in tryptophan catabolism and implicated in both maternal and T cell tolerance. Using quantitative assays to monitor levels of IDO mRNA, protein expression and enzyme activity, we report that PGE2 induces mRNA expression of IDO, however, a second signal through TNF-R or a TLR is necessary to activate the enzyme. Interestingly, use of TNF, lipopolysaccharide or SAC alone does not induce IDO. The effect of PGE2 is mediated by activation of adenylate cyclase via the Gs-protein coupled receptor E prostanoid-2 (EP2). A better understanding of these regulatory mechanisms and the cross-talk between TNF-R / TLR and EP2 signaling pathways will provide insight into the regulation of T cell activation by DCs and may help to improve existing immunotherapy protocols. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: IDO production, adaptive immunity, and CTL killing Thomas Luft, Eugene Maraskovsky, and Max Schnurr Blood 2005 106: 2228-2229. [Full Text] [PDF] This article has been cited by other articles: T. Onodera, M. H. Jang, Z. Guo, M. Yamasaki, T. Hirata, Z. Bai, N. M. Tsuji, D. Nagakubo, O. Yoshie, S. Sakaguchi, et al. Constitutive Expression of IDO by Dendritic Cells of Mesenteric Lymph Nodes: Functional Involvement of the CTLA-4/B7 and CCL22/CCR4 Interactions J. Immunol., November 1, 2009; 183(9): 5608 - 5614. [Abstract] [Full Text] [PDF] D. J. Chung, M. Rossi, E. Romano, J. Ghith, J. Yuan, D. H. Munn, and J. W. Young Indoleamine 2,3-dioxygenase-expressing mature human monocyte-derived dendritic cells expand potent autologous regulatory T cells Blood, July 16, 2009; 114(3): 555 - 563. [Abstract] [Full Text] [PDF] J. C. Schefold, J.-P. Zeden, C. 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