| Theme | Bone disorders in rheumatic diseases | |
|---|---|---|
| Title | Molecular mechanism of bone destruction in rheumatic diseases | |
| Publish Date | 2003/01 | |
| Author | Shigeru Kotake | Institute of Rheumatology, Tokyo Women's Medical University |
| [ Summary ] | Previously, we reported that IL-17 from activated human T cells in the synovial tissues of patients with rheumatoid arthritis (RA) is a potent stimulator of osteoclast formation via the synthesis of receptor activator of NF-KB ligand (RANKL) in osteoblasts. We also recently demonstrated that activated human T cells expressing RANKL directly induce the osteo clastogenesis from human monocytes. These findings suggested that excess production of RANKL by activated T cells increases the level of soluble RANKL (sRANKL) in the synovial fluid and may contribute to osteoclastic bone resorption in RA patients. Other groups also reported that activated T cells induce osteoclastogenesis through the same mechanisms, based on results involving murine cell cultures. Modulation of the RANKL expression by T cells may represent a useful direction for the development of new treatment strategies to inhibit bone destruction. | |