TNF-alpha induces osteoclastogenesis by direct stimulation of macrophages exposed to permissive levels of RANK ligand.
By Jonathan D. Lam, S. Takeshita, J. Barker, O. Kanagawa, F. Ross, S. Teitelbaum. Journal of Clinical Investigation, 2000
1,455 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology, Orthopedics and Sports Medicine
View Paper: https://www.semanticscholar.org/paper/70546681aaf08fb48a83043018b3d949de696a7c
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Citations in the corpus
- TSH is a negative regulator of skeletal remodeling. (2003, background): “On the other hand, mice rendered null for the 1 and thyroid hormone receptorsphorylated in response to TNF that regulates osteo- clast formation (Lam et al., 2000).”
- Inflammatory bone loss: pathogenesis and therapeutic intervention (2012, background): “In addition, under just permissive (subosteoclastogenic) concentrations of RANKL, TNF can induce the differentiation of monocytes and macrophages to the stage of preosteoclast”
- Induction of osteoclastogenesis and bone loss by human autoantibodies against citrullinated vimentin. (2012, positive): “TNF-α TNF-α , however, is also a major inducer of osteoclastogenesis by enhancing differentiation of osteoclasts and by trafficking of osteoclast precursors (21, 22).”
- Receptor activator of nuclear factor kappaB ligand and osteoprotegerin regulation of bone remodeling in health and disease. (2008, positive): “in vivo observations was provided when TNF- was shown to require very low “permissive” levels of RANKL to stimulate osteoclasts (116).”
- Mechanisms of TNF-α– and RANKL-mediated osteoclastogenesis and bone resorption in psoriatic arthritis (2003, positive): “Furthermore, it has been demonstrated that minuscule quantities of RANKL are sufficient to synergize with TNF-α and potentiate osteoclastogenesis (13).”
- IL-6, RANKL, TNF-alpha/IL-1: interrelations in bone resorption pathophysiology. (2004, background): “[75] have demonstrated that TNF- acts directly on osteoclast precursors to potentiate RANKL-induced osteoclastogenesis, even in the absence of elevated levels of RANKL.”
- IL-1 mediates TNF-induced osteoclastogenesis. (2005, methodology): “This observation is in keeping with the exquisite synergy enjoyed by TNF and RANKL and the fact that constitutive levels of the RANKL are sufficient to enable TNF’s osteoclastogenic properties (9).”
- Osteoimmunology: shared mechanisms and crosstalk between the immune and bone systems (2007, background): “Although TNF alone cannot induce osteoclastogenesis in vivo , nor can TNF overexpression rescue the deficiency of RANK”
- Genetic regulation of osteoclast development and function (2003, background): “Transplantation of bone marrow from wild-type mice into p55-TNFα-receptor −/− animals rescued these knockouts and so independently showed the crucial role of TNF&alpha”