对于我国现有约1.12亿骨质疏松症患者来说，弄清其主要病因肾虚的分子机制对其防治具有重大的意义。为此，课题组前期研究已证实CLCF1是绝经后骨质疏松症（PMOP）肾阴虚证的关联基因，可调控JAK2/STAT3信号通路，影响骨代谢。为厘清CLCF1对骨代谢的直接作用机制，本课题拟：①采用腺相关病毒敲低技术，观察CLCF1低表达对小鼠免疫及OPG/RANKL/RANK信号系统的影响；②B淋巴细胞和成骨细胞共培养，研究B淋巴细胞中CLCF1基因过表达和沉默对OPG/RANKL系统的影响；③分析六味地黄丸治疗PMOP肾阴虚证对免疫和OPG/RANKL/RANK系统的影响；从免疫系统与骨代谢的桥梁--OPG/RANKL/RANK信号系统探讨CLCF1调控骨代谢的机制，从而论证课题假说：“PMOP肾阴虚证的骨免疫机制可能与CLCF1调控OPG/RANKL/RANK信号系统影响骨代谢密切相关”的正确性。

For nearly 112 million patients with osteoporosis in China, it is of great significance for preventing and treating by clearly understanding the molecular mechanism of kidney deficiency. Thus, the research group has demonstrated in the earlier research that CLCF1 is an associated gene that can regulate JAK2/STAT3 signal pathway and impact bone metabolism for kidney yin deficiency of postmenopausal osteoporosis (PMOP). To make clear understanding of the direct-acting mechanism of CLCF1 for bone metabolism, this study intends to: ①observe impacts of low expression of CLCF1 upon immunities in mice and OPG/RANKL/RANK signal system using the technology of adenovirus associated virus. ②explore impacts of over-expression and silencing of CLCF1 on B lymphocytes by culcuturing the cells together with osteoblasts. ③ analyze the impacts of treating kidney yin deficiency of PMOP by Liuwei Dihuang pill upon immunities and OPG/RANKL/RANK system, and discuss the mechanism of regulating bone metabolism by CLCF1 by OPG/RANKL/RANK system via the bridge between immune system and bone metabolism, so as to demonstrate if the hypothesis of this study that “the molecular osteoimmunological mechanism of kidney yin deficiency of postmenopausal osteoporosis (PMOP) is possibly closely related to the impacts of CLCF1 regulation of OPG/RANKL/RANK signal system on bone metabolism” is right or not.