A signal through 4‐1BB ligand inhibits receptor for activation of nuclear factor‐κB ligand (RANKL)‐induced osteoclastogenesis by increasing interferon (IFN)‐beta production

Abstract
We tested whether any intracellular signals are transmitted through 4‐1BB/CD137 ligand (4‐1BBL), using a 4‐1BB‐Fc fusion protein and 4‐1BB‐deficient mice. Immobilized 4‐1BB‐Fc fusion protein strongly inhibited osteoclastogenesis induced by macrophage colony‐stimulating factor (M‐CSF) and receptor activator of nuclear factor‐κB ligand (RANKL) derived from bone marrow macrophages (BMM). Incubation of BMM with M‐CSF increased 4‐1BBL mRNA and surface expression of 4‐1BBL protein. Cross‐linking 4‐1BBL with immobilized 4‐1BB‐Fc also dramatically reduced the number of tartrate‐resistant acid phosphatase (TRAP)‐positive multinuclear cells (MNC) derived from the BMM from 4‐1BB‐deficient mice, suggesting that the inhibitory effect of immobilized 4‐1BB on osteoclastogenesis is due to a signal through 4‐1BBL. Reverse signaling by 4‐1BB‐Fc increased the level of interferon (IFN)‐β in BMM and neutralization of IFN‐β reversed the inhibitory effect of immobilized 4‐1BB‐Fc. Inhibition of osteoclastogenesis by immobilized 4‐1BB‐Fc is, therefore, at least in part, due to elevation of the level of the negative regulator, IFN‐β in BMM.

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