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Interaction of the Estrogen Receptors with the Fas Ligand Promoter in Human Monocytes

Gil Mor, Eva Sapi, Vikki M. Abrahams, Thomas Rutherford, Joon Song, Xiao-Ying Hao, Saeher Muzaffar and Fortune Kohen
J Immunol January 1, 2003, 170 (1) 114-122; DOI: https://doi.org/10.4049/jimmunol.170.1.114
Gil Mor
*Department of Obstetrics and Gynecology, School of Medicine, Yale University, New Haven, CT 06520;
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Eva Sapi
*Department of Obstetrics and Gynecology, School of Medicine, Yale University, New Haven, CT 06520;
†Department of Biology and Environmental Science, University of New Haven, West Haven, CT 06516;
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Vikki M. Abrahams
*Department of Obstetrics and Gynecology, School of Medicine, Yale University, New Haven, CT 06520;
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Thomas Rutherford
*Department of Obstetrics and Gynecology, School of Medicine, Yale University, New Haven, CT 06520;
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Joon Song
*Department of Obstetrics and Gynecology, School of Medicine, Yale University, New Haven, CT 06520;
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Xiao-Ying Hao
*Department of Obstetrics and Gynecology, School of Medicine, Yale University, New Haven, CT 06520;
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Saeher Muzaffar
*Department of Obstetrics and Gynecology, School of Medicine, Yale University, New Haven, CT 06520;
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Fortune Kohen
‡Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel
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Abstract

The predominance of autoimmune diseases among women suggests that estrogen may modulate immune function. Monocytes and macrophages are important in initiating, maintaining, and resolving inflammatory responses through cell-signaling molecules, which control immune cell survival. One important mechanism of cell survival is mediated by the Fas/Fas ligand (FasL) system. In this study, the link between estrogen, monocytes/macrophages, and the Fas/FasL system was investigated. Estrogen treatment increased FasL expression in monocytes through the binding of the estrogen receptors (ER) to the estrogen recognizing elements and AP-1 motifs present at the FasL promoter. Furthermore, estrogen induced apoptosis in monocytes expressing ERβ, but not in monocyte-differentiated macrophages expressing ERα. The expression of either ERα or ERβ and their response to estrogen in monocytes was found to be dependent on the their stage of cell differentiation. Previously, we have shown that estrogen replacement therapy in postmenopausal women decreased the number of circulating monocytes. In this study, we have characterized the molecular mechanism by which estrogen regulates monocytes homeostasis. These findings indicate that estrogen may regulate immune cell survival through the Fas/FasL system. There is biological relevance to these findings in view of studies showing that accumulation of activated monocytes is involved in the pathogenesis of conditions such as vasculititis, arteriosclerosis, and rheumatoid arthritis.

  • Received August 28, 2002.
  • Accepted October 28, 2002.
  • Copyright © 2003 by The American Association of Immunologists
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The Journal of Immunology: 170 (1)
The Journal of Immunology
Vol. 170, Issue 1
1 Jan 2003
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Interaction of the Estrogen Receptors with the Fas Ligand Promoter in Human Monocytes
Gil Mor, Eva Sapi, Vikki M. Abrahams, Thomas Rutherford, Joon Song, Xiao-Ying Hao, Saeher Muzaffar, Fortune Kohen
The Journal of Immunology January 1, 2003, 170 (1) 114-122; DOI: 10.4049/jimmunol.170.1.114

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Interaction of the Estrogen Receptors with the Fas Ligand Promoter in Human Monocytes
Gil Mor, Eva Sapi, Vikki M. Abrahams, Thomas Rutherford, Joon Song, Xiao-Ying Hao, Saeher Muzaffar, Fortune Kohen
The Journal of Immunology January 1, 2003, 170 (1) 114-122; DOI: 10.4049/jimmunol.170.1.114
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