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The role of dendritic cells derived osteoclasts in bone destruction diseases
Genes & Diseases ( IF 6.8 ) Pub Date : 2020-04-07 , DOI: 10.1016/j.gendis.2020.03.009
Bo Wang 1, 2 , Yutong Dong 1, 2 , Zhansong Tian 1 , Yueqi Chen 1, 3 , Shiwu Dong 1, 3, 4
Affiliation  

The bone is previously considered as a dominant organ involved in the processes of locomotion. However, in the past two decades, a large number of studies have suggested that the skeletal system closely coordinated with the immune system so as to result in the emerging area of ‘osteoimmunology’. In the evolution of many kinds of bone destruction-related diseases, osteoclasts could differentiate from dendritic cells, which contributed to increased expression of osteoclast-related membrane receptors and relatively higher activity of bone destruction, inducing severe bone destruction under inflammatory conditions. Numerous factors could influence the interaction between osteoclasts and dendritic cells, contributing to the pathogenesis of several bone diseases in the context of inflammation, including both immunocytes and a large number of cytokines. In addition, the products of osteoclasts released from bone destruction area serve as important signals for the differentiation and activation of immature dendritic cells. Therefore, the border between the dendritic cell-related immune response and osteoclast-related bone destruction has gradually unravelled. Dendritic cells and osteoclasts cooperate with each other to mediate bone destruction and bone remodelling under inflammatory conditions. In this review, we will pay attention to the interactions between dendritic cells and osteoclasts in physiological and pathological conditions to further understand the skeletal system and identify potential new therapeutic targets for the future by summarizing their significant roles and molecular mechanisms in bone destruction.



中文翻译:

树突状细胞衍生的破骨细胞在骨质破坏疾病中的作用

骨骼以前被认为是参与运动过程的主要器官。然而,近二十年来,大量研究表明骨骼系统与免疫系统密切配合,从而催生了“骨免疫学”这一新兴领域。在多种骨破坏相关疾病的演化过程中,破骨细胞可以分化为树突状细胞,导致破骨细胞相关膜受体表达增加,骨破坏活性相对较高,在炎症条件下引起严重的骨破坏。许多因素可能影响破骨细胞和树突状细胞之间的相互作用,从而导致炎症背景下多种骨疾病的发病机制,包括免疫细胞和大量细胞因子。此外,骨质破坏区域释放的破骨细胞产物是未成熟树突状细胞分化和激活的重要信号。因此,树突状细胞相关的免疫反应和破骨细胞相关的骨破坏之间的界限逐渐被阐明。树突状细胞和破骨细胞在炎症条件下相互配合介导骨破坏和骨重塑。在这篇综述中,我们将关注树突状细胞和破骨细胞在生理和病理条件下的相互作用,通过总结它们在骨破坏中的重要作用和分子机制,进一步了解骨骼系统并确定未来潜在的新治疗靶点。

更新日期:2020-04-07
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