IL‐17 induces osteoclastogenesis from human monocytes alone in the absence of osteoblasts, which is potently inhibited by anti‐TNF‐α antibody: A novel mechanism of osteoclastogenesis by IL‐17
- 2 September 2009
- journal article
- research article
- Published by Wiley in Journal of Cellular Biochemistry
- Vol. 108 (4), 947-955
- https://doi.org/10.1002/jcb.22326
Abstract
IL‐17 is a proinflammatory cytokine crucial for osteoclastic bone resorption in the presence of osteoblasts or synoviocytes in rheumatoid arthritis. However, the role of IL‐17 in osteoclastogenesis from human monocytes alone remains unclear. Here, we investigated the role of IL‐17 in osteoclastogenesis from human monocytes alone and the direct effect of infliximab on the osteoclastogenesis induced by IL‐17. Human peripheral blood mononuclear cells (PBMC) were cultured for 3 days with M‐CSF. After non‐adherent cells were removed, IL‐17 was added with either infliximab or osteoprotegerin (OPG). Seven days later, adherent cells were stained for vitronectin receptor. On the other hand, CD11b‐positive monocytes purified from PBMC were also cultured and stained as described above. CD11b‐positive cells were cultured with TNF‐α and receptor activator of NF‐κB ligand (RANKL). In the cultures of both adherent cells and CD11b‐positive cells, IL‐17 dose‐dependently induced osteoclastogenesis in the absence of soluble‐RANKL. OPG or infliximab inhibited IL‐17‐induced osteoclastogenesis. Interestingly, in the culture of CD11b‐positive cells, the osteoclastogenesis was more potently inhibited by infliximab than by OPG. TNF‐α and RANKL synergistically induced osteoclastogenesis. The present study clearly demonstrated the novel mechanism by which IL‐17 directly induces osteoclastogenesis from human monocytes alone. In addition, infliximab potently inhibits the osteoclastogenesis directly induced by IL‐17. J. Cell. Biochem. 108: 947–955, 2009.Keywords
This publication has 30 references indexed in Scilit:
- IL-23 induces human osteoclastogenesis via IL-17 in vitro, and anti-IL-23 antibody attenuates collagen-induced arthritis in ratsArthritis Research & Therapy, 2007
- Th17 functions as an osteoclastogenic helper T cell subset that links T cell activation and bone destructionThe Journal of Experimental Medicine, 2006
- A critical role for interleukin-6 family-mediated Stat3 activation in osteoblast differentiation and bone formationBone, 2006
- IL-23 drives a pathogenic T cell population that induces autoimmune inflammationThe Journal of Experimental Medicine, 2005
- The combination of tumor necrosis factor ? blockade with interleukin-1 and interleukin-17 blockade is more effective for controlling synovial inflammation and bone resorption in an ex vivo modelArthritis & Rheumatism, 2001
- IL-17 in synovial fluids from patients with rheumatoid arthritis is a potent stimulator of osteoclastogenesisJCI Insight, 1999
- Interleukin-18 (Interferon-γ–inducing Factor) Is Produced by Osteoblasts and Acts Via Granulocyte/Macrophage Colony-stimulating Factor and Not Via Interferon-γ to Inhibit Osteoclast FormationThe Journal of Experimental Medicine, 1997
- Chemical and physical properties of the extracellular matrix are required for the actin ring formation in osteoclastsJournal of Bone and Mineral Research, 1996
- Kinetics of the osteoclast cytoskeleton during the resorption cycle in vitroJournal of Bone and Mineral Research, 1991
- Detection of tumor necrosis factor α but not tumor necrosis factor β in rheumatoid arthritis synovial fluid and serumArthritis & Rheumatism, 1988