d that increased expression of CIITA leads to expanded antigen presentation by macrophages immune cells that alert T cells to the presence of invading organisms and enhanced T cell activation in the bone marrow and extended T-cell lifespan. IFN-g has previously been implicated as an activator of aberrant immune expression in autoimmune diseases.

"This study represents a major advance in our understanding of the mechanism of action of estrogen in bone, including the essential link between the immune system and bone stability," said Dr. Pacifici. "If we observe the same results in humans, this could lead to the development of new drugs that work in bone like estrogen, but do not have negative effects on reproductive organs and the cardiovascular system. The study also helps explain why certain autoimmune diseases, such as rheumatoid arthritis, are improved by estrogen and exacerbated by menopause."

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Contact: Holly Korschun
hkorsch@emory.edu
404-727-3990
Emory University Health Sciences Center
4-Aug-2003

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