Tumor Necrosis Factor α Stimulates Osteoclast Differentiation by a Mechanism Independent of the Odf/Rankl–Rank Interaction

Journal of Experimental Medicine - Tập 191 Số 2 - Trang 275-286 - 2000
Kanichiro Kobayashi1, Naoyuki Takahashi1, Eijiro Jimi1, Nobuyuki Udagawa1, Masamichi Takami1, Shigeru Kotake2, N. Nakagawa3, Masahiko Kinosaki3, Kyoji Yamaguchi3, Nobuyuki Shima3, Hisataka Yasuda3, Tomonori Morinaga3, Kanji Higashio3, T. John Martin4, Tatsuo Suda1
1aDepartment of Biochemistry, School of Dentistry, Showa University, Tokyo 142-8555, Japan
2bThe Institute of Rheumatology, Tokyo Women's Medical University, Tokyo 162-0054, Japan
3cResearch Institute of Life Science, Snow Brand Milk Products Co., Ltd., Tochigi 329-0512, Japan
4dSt. Vincent's Institute of Medical Research, Fitzroy, Victoria 3065, Australia

Tóm tắt

Osteoclast differentiation factor (ODF, also called RANKL/TRANCE/OPGL) stimulates the differentiation of osteoclast progenitors of the monocyte/macrophage lineage into osteoclasts in the presence of macrophage colony-stimulating factor (M-CSF, also called CSF-1). When mouse bone marrow cells were cultured with M-CSF, M-CSF–dependent bone marrow macrophages (M-BMMφ) appeared within 3 d. Tartrate-resistant acid phosphatase–positive osteoclasts were also formed when M-BMMφ were further cultured for 3 d with mouse tumor necrosis factor α (TNF-α) in the presence of M-CSF. Osteoclast formation induced by TNF-α was inhibited by the addition of respective antibodies against TNF receptor 1 (TNFR1) or TNFR2, but not by osteoclastogenesis inhibitory factor (OCIF, also called OPG, a decoy receptor of ODF/RANKL), nor the Fab fragment of anti–RANK (ODF/RANKL receptor) antibody. Experiments using M-BMMφ prepared from TNFR1- or TNFR2-deficient mice showed that both TNFR1- and TNFR2-induced signals were important for osteoclast formation induced by TNF-α. Osteoclasts induced by TNF-α formed resorption pits on dentine slices only in the presence of IL-1α. These results demonstrate that TNF-α stimulates osteoclast differentiation in the presence of M-CSF through a mechanism independent of the ODF/RANKL–RANK system. TNF-α together with IL-1α may play an important role in bone resorption of inflammatory bone diseases.

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Journal of Experimental Medicine

Tập 191 Số 2

275-286

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