T-Cell Lifespan Linked to Postmenopausal Bone Loss

Researchers have identified the molecular mechanism that links the prolonged lifespan of immune T-cells to the postmenopausal loss of bone resulting from estrogen deficiency.

In order to study postmenopausal estrogen deficiency, investigators at Emory University (Atlanta, GA, USA) removed the ovaries from mice, and then studied T-cells from these animals in culture.

They found that T-cell activation was triggered by the up regulation of interferon gamma (IFN-g) stimulated class II transactivator (CIITA). Increased expression of CIITA led to expanded antigen presentation by macrophages, enhanced T-cell activation in the bone marrow, and extended T-cell lifespan. These findings were published August 15, 2003, in the on-line edition of the Proceedings of the National Academy of Sciences.

"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,” explained senior author Dr. Roberto Pacifici, professor of medicine at Emory University. "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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