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Blood, 15 March 2005, Vol. 105, No. 6, pp. 2415-2420. Prepublished online as a Blood First Edition Paper on September 21, 2004; DOI 10.1182/blood-2004-07-2819. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-07-2819v1 105/6/2415    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Gourdy, P. Articles by Herbelin, A. Search for Related Content PubMed PubMed Citation Articles by Gourdy, P. Articles by Herbelin, A. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Relevance of sexual dimorphism to regulatory T cells: estradiol promotes IFN- production by invariant natural killer T cells Pierre Gourdy, Luiza M. Araujo, Ren Zhu, Barbara Garmy-Susini, Séverine Diem, Henrik Laurell, Maria Leite-de-Moraes, Michel Dy, Jean François Arnal, Francis Bayard, and André Herbelin From the Institut National de la Santé et de la Recherche Médicale (INSERM) U589, Institut L. Bugnard, Centre Hospitalier et Universitaire (CHU) Rangueil, Toulouse, France, and the Centre National de la Recherche Scientifique (CNRS) Unité Mixte de Recherche (UMR) 8147 and Paris V, Hôpital Necker, Paris, France. Mechanisms accounting for gender dimorphism during immune responses are still poorly understood. Since invariant natural killer T (iNKT) cells exert important regulatory functions through their capacity to produce both T helper 1 (Th1) and Th2 cytokines, we addressed the question of whether these activities could be modulated by sexual hormones. We found that in vivo challenge with the specific ligand of iNKT cells, -galactosylceramide (-GalCer), induced significantly higher concentrations of interferon (IFN-) in the serum of female than in that of male mice, while interleukin 4 (IL-4) production was not modified. In support of a crucial role of ovarian hormones in this phenomenon, a significant decrease of serum IFN- concentrations occurred in ovariectomized females, in response to treatment with -GalCer, while orchidectomy affected neither IFN- nor IL-4 serum concentrations in males. The implication of estrogens in this selective enhancement of IFN- production by iNKT cells was demonstrated by (1) the increased -GalCer–induced IFN- synthesis by iNKT cells upon both in vitro and in vivo exposure to estradiol and (2) the abolition of the sex-linked difference in -GalCer–induced IFN- release in estrogen receptor -deficient mice. These results provide the first evidence that estrogens influence iNKT cells leading to this gender dimorphism in their cytokine production profile. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: R. Dai, R. A. Phillips, E. Karpuzoglu, D. Khan, and S. A. Ahmed Estrogen Regulates Transcription Factors STAT-1 and NF-{kappa}B to Promote Inducible Nitric Oxide Synthase and Inflammatory Responses J. Immunol., December 1, 2009; 183(11): 6998 - 7005. [Abstract] [Full Text] [PDF] S. Radom-Aizik, F. Zaldivar Jr., S.-Y. Leu, and D. M. 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