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* 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;
Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel
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 ER
, but not in
monocyte-differentiated macrophages expressing ER
. The expression of
either ER or ER 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.
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