Regulation of osteoclastogenesis by activated T cells

Bone destruction in rheumatoid arthritis (RA) is caused by osteoclasts, multinuclear cells of the monocyte/macrophage lineage. Since osteoclast differentiation factor RANKL (receptor activator of NF-kappaB ligand) is expressed on activated T cells and T cells, especially Th1 type cells, are implicated in the pathogenesis of RA, it has been believed that they play an important role in the osteoclastogenesis in RA lesions. However, main Th1-type cytokine IFN-gamma strongly suppresses osteoclastogenesis, casting doubt on the relevancy of Th1 cells as stimulators of osteoclastogenesis. Recently, IL-17 from T cells has been reported to enhance osteoclastogenesis. Characterizing real Th subsets which support osteoclastogenesis would be beneficial to solving a clinically important problem, bone destruction in RA.