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t cells and post menopausal osteoporosis in murine models在小鼠模型中t细胞和绝经后骨质疏松症
Available online /content/9/2/102
Commentary
T cells and post menopausal osteoporosis in murine models
Roberto Pacifici
Division of Endocrinology, Metabolism and Lipids, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA
Corresponding author: Roberto Pacifici, roberto.pacifici@
Published: 5 March 2007 Arthritis Research Therapy 2007, 9:102 (doi:10.1186/ar2126)
This article is online at /content/9/2/102
© 2007 BioMed Central Ltd
Abstract stimulated osteoblastogenesis fueled by an expansion of the
Estrogen deficiency is one of the most frequent causes of pool of early mesenchymal progenitors, and by increased
osteoporosis in women and a possible cause of bone loss in men. commitment of such pluripotent precursors toward the
But the mechanism involved remains largely unknown. Estrogen osteoblastic lineage [4]. In spite of stimulated osteoblasto-
deficiency leads to an increase in the immune function, which genesis, the net increase in bone formation is inadequate to
culminates in an increased production of tumor necrosis factor compensate for enhanced bone resorption because of an
(TNF) by activated T cells. TNF increases osteoclast formation and
augmentation in osteoblast (OB) apoptosis, a phenomenon
bone resorption both directly and by augmenting the sensitivity of
maturing osteoclasts to the essential osteoclastogenic factor also induced by estrogen deficiency [5]. An additional event
RANKL
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