摘要
绝经后骨质疏松症(postmenopausal osteoporosis,PMOP)是由绝经期雌激素缺乏引起的骨代谢紊乱相关的全身性骨骼疾病。主要组织相容性复合体Ⅱ类分子(major histocompatibility complex ClassⅡmolecules,MHC-Ⅱ)是蛋白质呈递途径的核心,其功能受雌激素调节,可通过参与由T和B淋巴细胞介导的适应性免疫反应,促进T细胞衍生各种炎症因子,最终促进破骨细胞介导的骨骼的骨形成和骨吸收。笔者就雌激素、MHC-Ⅱ、淋巴细胞及其在破骨细胞分化过程及功能活性中的潜在机制进行综述,进而更好地理解MHC-Ⅱ在绝经后骨质疏松症中的可能作用。
Postmenopausal osteoporosis(PMOP)is a systemic skeletal disorder associated with disturbances in bone metabolism caused by estrogen deficiency during menopause.Major histocompatibility complex class II molecules(MHC-II),central to the protein presentation pathway,are regulated by estrogen and can participate in the adaptive immune response mediated by T and B lymphocytes and promote T cell-derived inflammatory factors,which ultimately promote osteoclast-mediated bone formation and bone resorption in the skeleton.In this paper,to better understand the possible role of MHC-II in postmenopausal osteoporosis,we review estrogen,MHC-II,and lymphocytes,and their potential mechanisms in the differentiation process and functional activity of osteoclasts.
作者
张桢
陈昊
王雪鹏
朱六龙
ZHANG Zhen;CHEN Hao;WANG Xuepeng;ZHU Liulong(Department of Orthopedics Surgery,Affiliated Hangzhou First People’s Hospital,Zhejiang University School of Medicine,Hangzhou 310006,China)
出处
《中国骨质疏松杂志》
CAS
CSCD
北大核心
2024年第2期270-274,共5页
Chinese Journal of Osteoporosis
基金
浙江省基础公益研究计划项目(LGF21H060004,LGF22H060025)
浙江省医药卫生科技计划项目(2022519575,2023KY175)。
