Shigeru Kotake

TL;DR: It is suggested that IL-17 first acts on osteoblasts, which stimulates both COX-2-dependent PGE2 synthesis and ODF gene expression, which in turn induce differentiation of osteoclast progenitors into mature osteoclasts, and that IL -17 is a crucial cytokine for osteoclastic bone resorption in RA patients.

TL;DR: It is demonstrated that TNF-α stimulates osteoclast differentiation in the presence of M-CSF through a mechanism independent of the ODF/RANKL–RANK system.

TL;DR: Results suggest that IL‐6 in the RA synovial fluids is at least in part responsible for joint destruction in the presence of sIL‐6R through osteoclastogenesis.

TL;DR: The present findings suggest that excess production of RANKL by activated T cells increases the level of sRANKL in synovial fluid and may contribute to osteoclastic bone resorption in RA patients, the first to demonstrate osteoclastogenesis using human-derived T cells and monocytes.

TL;DR: It is demonstrated that IL-23 stimulates the differentiation of human osteoclasts from peripheral blood mononuclear cells (PBMC) and in vivo blockade of endogenous IL- 23 activity by treatment with anti-IL-23 antibody attenuates collagen-induced arthritis in rats by preventing both inflammation and bone destruction.