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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.

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IMMUNOBIOLOGY

17{beta}-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{beta}-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{beta} (MIP3{beta}). 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.


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