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Blood, 1 September 2004, Vol. 104, No. 5, pp. 1404-1410. Prepublished online as a Blood First Edition Paper on May 13, 2004; DOI 10.1182/blood-2003-10-3380. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-10-3380v1 104/5/1404    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 Bengtsson, A. K. Articles by Clark, E. A. Search for Related Content PubMed PubMed Citation Articles by Bengtsson, A. K. Articles by Clark, E. A. Related Collections Immunobiology Phagocytes Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY 17-Estradiol (E2) modulates cytokine and chemokine expression in human monocyte-derived dendritic cells Åsa K. Bengtsson, Elizabeth J. Ryan, Daniela Giordano, Dario M. Magaletti, and Edward A. Clark From the Departments of Microbiology and Immunology and the Regional Primate Research Center, University of Washington, Seattle. The effects of estrogen on the immune system are still largely unknown. We have investigated the effect of 17-estradiol (E2) on human monocyte-derived immature dendritic cells (iDCs). Short-term culture in E2 had no effect on iDC survival or the expression of cell surface markers. However, E2 treatment significantly increased the secretion of interleukin 6 (IL-6) in iDCs and also increased secretion of osteoprotegerin (OPG) by DCs. Furthermore, E2 significantly increased secretion of the inflammatory chemokines IL-8 and monocyte chemoattractant protein 1 (MCP-1) by iDCs, but not the production of the constitutive chemokines thymus and activation-regulated chemokine (TARC) and macrophage-derived chemokine (MDC). However, after E2 pretreatment the lipopolysaccharide (LPS)–induced production of MCP-1, TARC, and MDC by DCs was clearly enhanced. Moreover, mature DCs pretreated with E2 stimulated T cells better than control cells. Finally, we found that E2 provides an essential signal for migration of mature DCs toward CCL19/macrophage inflammatory protein 3 (MIP3). In summary, E2 may affect DC regulation of T-cell and B-cell responses, as well as help to sustain inflammatory responses. This may explain, in part, the reason serum levels of estrogen correlate with the severity of certain autoimmune diseases. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? 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