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Estrogen receptors interact with the Fas ligand promoter in human monocytes.

Women's Health Weekly

| March 06, 2003 | COPYRIGHT 2003 NewsRX. This material is published under license from the publisher through the Gale Group, Farmington Hills, Michigan.  All inquiries regarding rights should be directed to the Gale Group. (Hide copyright information)Copyright

2003 MAR 6 - (NewsRx.com & NewsRx.net) -- According to a study from the United States, "The predominance of autoimmume 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/ras ligand (FasL) system," stated G. Mor and coauthors, Yale University School of Medicine.

"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 ERbeta, but not in monocyte-differentiated macrophages expressing ERalpha.

"The expression of either ERalpha or ERbeta and their response to estrogen in monocytes was found to be dependent on 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 ...

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