The immune and skeletal systems share a variety of molecules, including cytokines, chemokines, hormones, receptors, and transcription factors. Bone cells interact with immune cells under physiological and pathological conditions. Osteoimmunology was created as a new interdisciplinary field in large part to highlight the shared molecules and reciprocal interactions between the two systems in both heath and disease. Receptor activator of NF-κB ligand (RANKL) plays an essential role not only in the development of immune organs and bones, but also in autoimmune diseases affecting bone, thus effectively comprising the molecule that links the two systems. Here we review the function, gene regulation, and signal transduction of osteoimmune molecules, including RANKL, in the context of osteoclastogenesis as well as multiple other regulatory functions. Osteoimmunology has become indispensable for understanding the pathogenesis of a number of diseases such as rheumatoid arthritis (RA). We review the various osteoimmune pathologies, including the bone destruction in RA, in which pathogenic helper T cell subsets [such as IL-17-expressing helper T (Th17) cells] induce bone erosion through aberrant RANKL expression. We also focus on cellular interactions and the identification of the communication factors in the bone marrow, discussing the contribution of bone cells to the maintenance and regulation of hematopoietic stem and progenitors cells. Thus the time has come for a basic reappraisal of the framework for understanding both the immune and bone systems. The concept of a unified osteoimmune system will be absolutely indispensable for basic and translational approaches to diseases related to bone and/or the immune system.

中文翻译：

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骨免疫学：统一免疫和骨骼系统的概念框架

免疫系统和骨骼系统共享各种分子，包括细胞因子，趋化因子，激素，受体和转录因子。在生理和病理条件下，骨细胞与免疫细胞相互作用。骨免疫学被创建为一个新的交叉学科领域，在很大程度上突出了在健康和疾病两个系统之间共享的分子和相互的相互作用。NF-κB配体的受体激活剂（RANKL）不仅在免疫器官和骨骼的发育中起着重要作用，而且在影响骨骼的自身免疫性疾病中也起着至关重要的作用，因此有效地组成了连接这两个系统的分子。在这里，我们回顾了破骨细胞形成以及其他多种调控功能中，包括RANKL在内的骨免疫分子的功能，基因调控和信号转导。骨免疫学已成为了解许多疾病（如类风湿关节炎（RA））的发病机理所不可或缺的。我们审查了各种骨免疫病理学，包括RA中的骨破坏，其中致病性辅助T细胞亚群（例如表达IL-17的辅助T（Th17）细胞）通过异常的RANKL表达诱导骨侵蚀。我们还将重点放在骨髓中的细胞相互作用和通讯因子的识别上，讨论骨细胞对造血干细胞和祖细胞维持和调节的贡献。因此，现在是对评估免疫系统和骨骼系统的框架进行基本重新评估的时候了。