Liu Yen Chun G, Teng Andy Yen-Tung
Center for Osteo-immunology & Biotechnology Research (COBR) and Department of Dental Hygiene, College of Dental Medicine, Kaohsiung Medical University, Kaohsiung City, Taiwan.
Center for Osteo-immunology & Biotechnology Research (COBR), School of Dentistry, College of Dental Medicine, Kaohsiung Medical University (KMU) and KMU-Hospital, Kaohsiung City, Taiwan.
J Dent Sci. 2023 Jul;18(3):1372-1377. doi: 10.1016/j.jds.2023.03.016. Epub 2023 Apr 5.
Dendritic cells (DC) are potent antigen-presenting-cells widely distributed at the osteo-immune and/or mucosal-mesenchyme interface, consequentially implicating in certain bone-sparing disorders; i.e., via signaling Receptor-activator-of-nuclear-factor-kappa-B-ligand/RANKL-Receptor-activator-of-nuclear-factor-kB/RANK-Osteoprotegerin/OPG-TRAF6 transducer-complex , evidently associated with arthritis, osteoporosis and periodontitis. We have reported that the immature myeloid CD11c-DC subsets can act as osteoclast precursor (OCp; mDDOCp), thereby developing into osteoclasts (OCs) via an alternative pathway for osteoclastogenesis. Importantly, cytokine TGF-β remains critical to prime CD11c-mDDOCp-cells deficient of TRAF6-&-related immune/osteotropic signaling, featuring distinctive TGF-β-&-IL-17-invoked effectors in the environmental milieu sufficient to driving bona-fide osteoclastogenesis . Herein, we sought to explore the potential contribution of immature-mDDOCp/OCp to inflammation-induced bone-loss, where comparable CD11cTRAPmultinucleated-OC-like/mDDOCp existed, lacking the endogenous TRAF6-associated monocyte/macrophage-derived OCs in type-II-collagen induced joint/paw inflammation of the C56BL/6-TRAF6null chimeras (H-2-halpotype) examined. The results suggest that such TRAF6-null chimeric mice may offer a useful model to assess the specific functions of OCp or mDDOCp as an analog to human conditions .
树突状细胞（DC）是强大的抗原呈递细胞，广泛分布于骨免疫和/或粘膜间充质界面，因此与某些骨质保护疾病有关；即通过信号传导核因子κB受体激活剂配体/核因子κB受体激活剂/核因子κB受体激活剂/骨保护素/OPG-TRAF6转导复合物，显然与关节炎、骨质疏松症和牙周炎有关。我们已经报道，未成熟的髓样CD11c-DC亚群可以作为破骨细胞前体（OCp；mDDOCp），从而通过破骨细胞生成的替代途径发育为破骨细胞（OCs）。重要的是，细胞因子TGF-β对于启动缺乏TRAF6及相关免疫/骨营养信号的CD11c-mDDOCp细胞仍然至关重要，在足以驱动真正破骨细胞生成的环境中，具有独特的TGF-β和IL-17激活的效应器。在此，我们试图探索未成熟的mDDOCp/OCp对炎症诱导的骨质流失的潜在贡献，在检查的C56BL/6-TRAF6基因敲除嵌合体（H-2单倍型）的II型胶原诱导的关节/爪炎症中，存在可比的CD11cTRAP多核OC样/mDDOCp，缺乏内源性TRAF6相关的单核细胞/巨噬细胞衍生的OCs。结果表明，这种TRAF6基因敲除嵌合小鼠可能为评估OCp或mDDOCp作为人类疾病类似物的特定功能提供一个有用的模型。
