Dendritic cells at the osteo-immune interface: Implications for inflammation-induced bone loss
Dendritic cells at the osteo-immune interface: Implications for inflammation-induced bone loss
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DOI：
10.1359/jbmr.070314
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发表时间：
2007-06-01
影响因子：
6.2
通讯作者：
Teng, Yen-Tung A.
中科院分区：
文献类型：
--
作者：
Alnaeeli, Mawadda;Park, Jaekweon;Teng, Yen-Tung A.
在过去的十年中，T细胞和T细胞介导的免疫在炎症诱导的破骨细胞生成和随后的骨丢失中的关键作用已被广泛研究，从而建立了骨免疫学的新范式。因此，树突状细胞（DC），最有效的抗原呈递细胞，负责激活幼稚T细胞和协调免疫反应，成为关键位于骨免疫界面。如今，新出现的证据表明，DC可能直接参与炎症诱导的破骨细胞生成和骨丢失，作为破骨细胞（OC）的前体，可以进一步发展成DC衍生的OC（DDOC）在炎症条件下。这些发现具有巨大的意义，因为除了DC在调节先天性和适应性免疫中的重要作用外，这些细胞对炎症诱导的骨丢失的直接贡献可能不仅为控制炎症而且还为调节骨破坏提供有希望的治疗靶点。
Within the past decade, the critical roles of T cells and T cell-mediated immunity in inflammation-induced osteoclastogenesis and subsequent bone loss have been extensively studied, thereby establishing the new paradigm of osteoimmunology. Therefore, dendritic cells (DCs), the most potent antigen-presenting cells, responsible for activation of naive T cells and orchestration of the immune response, became critically situated at the osteo-immune interface. Today, emerging new evidence suggests that DC may be directly involved in inflammation-induced osteoclastogenesis and bone loss, by acting as osteoclast (OC) precursors that can further develop into DC-derived OCs (DDOC) under inflammatory conditions. These findings have tremendous implications, because in addition to DC's important roles in regulating innate and adaptive immunity, a direct contribution by these cells to inflammation-induced bone loss may provide a promising therapeutic target not only for controlling inflammation but also for modulating bone destruction.