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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 (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 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 Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted October 1, 2003 Accepted April 27, 2004 17--estradiol (E2) modulates cytokine and chemokine expression in human monocyte-derived dendritic cells Asa K Bengtsson*, Elizabeth J Ryan, Daniela Giordano, Dario M Magaletti, and Edward A Clark Microbiology, University of Washington, Seattle, WA, USA; Immunology, University of Washington, Seattle, WA, USA Microbiology, University of Washington, Seattle, WA, USA; Regional Primate Research Center, University of Washington, Seattle, WA, USA Immunology, University of Washington, Seattle, WA, USA Regional Primate Research Center, University of Washington, Seattle, WA, USA Microbiology, University of Washington, Seattle, WA, USA; Immunology, University of Washington, Seattle, WA, USA; Regional Primate Research Center, University of Washington, Seattle, WA, USA * Corresponding author; email: asab{at}u.washington.edu. 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 IL-6 in iDCs, and also increased secretion of OPG by DCs. Furthermore, E2 significantly increased secretion of the inflammatory chemokines IL-8 and MCP-1 by iDCs, but not the production of the constitutive chemokines TARC and MDC. However, after E2 pretreatment the 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 towards CCL19/MIP3. In summary, E2 may impact DC regulation of T cell and B cell responses, as well as help to sustain inflammatory responses. 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