17β-Estradiol (E2) modulates cytokine and chemokine expression in human monocyte-derived dendritic cells

• Published in: Blood Vol. 104; no. 5; pp. 1404 - 1410
• Main Authors: Bengtsson, Åsa K., Ryan, Elizabeth J., Giordano, Daniela, Magaletti, Dario M., Clark, Edward A.
• Format: Journal Article
• Language: English
• Published: Washington, DC Elsevier Inc 01.09.2004; The Americain Society of Hematology
• Subjects: Biological and medical sciences; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Immunobiology; Modulation of the immune response (stimulation, suppression); Human; Immunopathology; Dendritic cell; Immune response; Monocyte; Estrogen; Cytokine; 17β-Estradiol; Autoimmune disease; Immune regulation; Ovarian hormone; Chemokine; Antigen presenting cell; Sex steroid hormone
• ISSN: 0006-4971; 1528-0020
• DOI: 10.1182/blood-2003-10-3380

The effects of estrogen on the immune system are still largely unknown. We have investigated the effect of 17β-estradiol (E2) on human monocyte-derived immature dendritic cells (iDCs). Short-term culture in E2had no effect on iDC survival or the expression of cell surface markers. However, E2treatment significantly increased the secretion of interleukin 6 (IL-6) in iDCs and also increased secretion of osteoprotegerin (OPG) by DCs. Furthermore, E2significantly 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 E2pretreatment the lipopolysaccharide (LPS)–induced production of MCP-1, TARC, and MDC by DCs was clearly enhanced. Moreover, mature DCs pretreated with E2stimulated T cells better than control cells. Finally, we found that E2provides an essential signal for migration of mature DCs toward CCL19/macrophage inflammatory protein 3β (MIP3β). In summary, E2may 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.