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首页> 外文期刊>Annals of the New York Academy of Sciences >Estrogen Regulation of Immune Cell Bone Interactions
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Estrogen Regulation of Immune Cell Bone Interactions

机译:免疫细胞骨骼相互作用的雌激素调节

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摘要

Estrogen deficiency is one of the most frequent causes of osteoporosis in women and a possible cause of bone loss and insufficient skeletal development in men. Estrogen deficiency results from menopause but also by a number of conditions, such as stress, excessive physical activity, and low body weight. The mechanism by which estrogen deficiency causes bone loss remains largely unknown. Estrogen deficiency leads to an increase in the immune function, which culminates in an increased production of TNF by activated T cells. TNF increases os-teoclast formation and bone resorption both directly and by augmenting the sensitivity of maturing osteoclasts to the essential osteoclastogenic factor RANKL. Increased T cell production of TNF is induced by estrogen deficiency via a complex mechanism mediated by antigen-presenting cells and involving the cytokines IFN-γ, IL-7, and TGF-β. Herein we review the experimental evidence that suggests that estrogen prevents bone loss by regulating T cell function and immune cell bone interactions.
机译:雌激素缺乏是女性骨质疏松症最常见的原因之一,也是男性骨质流失和骨骼发育不足的可能原因。雌激素缺乏症是由更年期引起的,也可能是由许多情况引起的,例如压力,过度的体育活动和体重过轻。雌激素缺乏导致骨质流失的机制仍然未知。雌激素缺乏导致免疫功能增强,最终导致活化T细胞产生的TNF增加。 TNF直接或通过增加成熟破骨细胞对必需破骨细胞生成因子RANKL的敏感性来增加破骨细胞的形成和骨吸收。雌激素缺乏通过抗原呈递细胞介导并涉及细胞因子IFN-γ,IL-7和TGF-β的复杂机制诱导TNF的T细胞产量增加。本文中,我们回顾了表明雌激素通过调节T细胞功能和免疫细胞骨骼相互作用来预防骨质流失的实验证据。

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