Potential contribution of immature myeloid CD11c+dendritic cells-derived osteoclast precursor to inflammation-induced bone loss in the TRAF6-null chimeras in-vivo
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-nucl...
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| Format: | Article |
| Language: | English |
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Elsevier
2023-07-01
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| Series: | Journal of Dental Sciences |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S1991790223000909 |
| _version_ | 1797808416523026432 |
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| author | Yen Chun G. Liu Andy Yen-Tung Teng |
| author_facet | Yen Chun G. Liu Andy Yen-Tung Teng |
| author_sort | Yen Chun G. Liu |
| collection | DOAJ |
| description | 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 etc., 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 in-vitro. Herein, we sought to explore the potential contribution of immature-mDDOCp/OCp to inflammation-induced bone-loss, where comparable CD11c+TRAP+multinucleated-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-TRAF6(−/−)null chimeras (H-2b-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 in-vivo. |
| first_indexed | 2024-03-13T06:37:09Z |
| format | Article |
| id | doaj.art-84b0db4449804602af9be79657b40009 |
| institution | Directory Open Access Journal |
| issn | 1991-7902 |
| language | English |
| last_indexed | 2024-03-13T06:37:09Z |
| publishDate | 2023-07-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Journal of Dental Sciences |
| spelling | doaj.art-84b0db4449804602af9be79657b400092023-06-09T04:27:37ZengElsevierJournal of Dental Sciences1991-79022023-07-0118313721377Potential contribution of immature myeloid CD11c+dendritic cells-derived osteoclast precursor to inflammation-induced bone loss in the TRAF6-null chimeras in-vivoYen Chun G. Liu0Andy Yen-Tung Teng1Center for Osteo-immunology & Biotechnology Research (COBR) and Department of Dental Hygiene, College of Dental Medicine, Kaohsiung Medical University, Kaohsiung City, TaiwanCenter for Osteo-immunology & Biotechnology Research (COBR), School of Dentistry, College of Dental Medicine, Kaohsiung Medical University (KMU) and KMU-Hospital, Kaohsiung City, Taiwan; Lab of Molecular Microbial Immunity and Div. of Periodontology, The Eastman Institute for Oral Health (EIOH), School of Medicine & Dentistry, University of Rochester, Rochester, NY, USA; Corresponding author. The Eastman Institute for Oral Health (EIOH), School of Medicine & Dentistry, University of Rochester, 625 Elmwood Ave., Rochester, NY, 14620, USA.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 etc., 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 in-vitro. Herein, we sought to explore the potential contribution of immature-mDDOCp/OCp to inflammation-induced bone-loss, where comparable CD11c+TRAP+multinucleated-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-TRAF6(−/−)null chimeras (H-2b-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 in-vivo.http://www.sciencedirect.com/science/article/pii/S1991790223000909Osteoclast & osteoclastogenesisDendritic cells (DCs) & myeloid dendritic cell-derived osteoclast precursors (mDDOCp)Inflammation-induced bone lossTRAF6 & TGF-β signalingImmune-osteotropic cytokines |
| spellingShingle | Yen Chun G. Liu Andy Yen-Tung Teng Potential contribution of immature myeloid CD11c+dendritic cells-derived osteoclast precursor to inflammation-induced bone loss in the TRAF6-null chimeras in-vivo Journal of Dental Sciences Osteoclast & osteoclastogenesis Dendritic cells (DCs) & myeloid dendritic cell-derived osteoclast precursors (mDDOCp) Inflammation-induced bone loss TRAF6 & TGF-β signaling Immune-osteotropic cytokines |
| title | Potential contribution of immature myeloid CD11c+dendritic cells-derived osteoclast precursor to inflammation-induced bone loss in the TRAF6-null chimeras in-vivo |
| title_full | Potential contribution of immature myeloid CD11c+dendritic cells-derived osteoclast precursor to inflammation-induced bone loss in the TRAF6-null chimeras in-vivo |
| title_fullStr | Potential contribution of immature myeloid CD11c+dendritic cells-derived osteoclast precursor to inflammation-induced bone loss in the TRAF6-null chimeras in-vivo |
| title_full_unstemmed | Potential contribution of immature myeloid CD11c+dendritic cells-derived osteoclast precursor to inflammation-induced bone loss in the TRAF6-null chimeras in-vivo |
| title_short | Potential contribution of immature myeloid CD11c+dendritic cells-derived osteoclast precursor to inflammation-induced bone loss in the TRAF6-null chimeras in-vivo |
| title_sort | potential contribution of immature myeloid cd11c dendritic cells derived osteoclast precursor to inflammation induced bone loss in the traf6 null chimeras in vivo |
| topic | Osteoclast & osteoclastogenesis Dendritic cells (DCs) & myeloid dendritic cell-derived osteoclast precursors (mDDOCp) Inflammation-induced bone loss TRAF6 & TGF-β signaling Immune-osteotropic cytokines |
| url | http://www.sciencedirect.com/science/article/pii/S1991790223000909 |
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