IL-1 mediates TNF-induced osteoclastogenesis.

By S. Wei, H. Kitaura, Ping Zhou, F. Ross, S. Teitelbaum. Journal of Clinical Investigation, 2005

791 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/26a026b16098524f0c42a3e5f00f4f7526b54e1d

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. S. Teitelbaum

In Molecular Biology

1. F. Bäckhed
2. S. Khosla
3. Georg Schett
4. V. Tremaroli
5. I. McInnes
6. P. Kostenuik
7. A. Kearns
8. S. Teitelbaum

In Oncology

1. I. McInnes
2. Georg Schett
3. S. Khosla
4. P. Kostenuik
5. A. Kearns
6. S. Teitelbaum
7. F. Bäckhed
8. S. Gaffen

Citations in the corpus

• Cytokines in the pathogenesis of rheumatoid arthritis (2007, background): “Moreover, IL-1β is a key component of TNF-mediated osteoclastogenesis; TNF induces IL-1 and IL-1R expression by mesenchymal cells and cells of the osteoclast lineage, which subsequently support the RANKL–RANK syste”
• Receptor activator of nuclear factor kappaB ligand and osteoprotegerin regulation of bone remodeling in health and disease. (2008, positive): “Many molecules that suppress osteoclastogenesis and/or bone resorption have also been shown to regulate OPG and/or RANKL, including estrogen (46, 76, 84, 104–108), interferon- (52), TGF- (52), IL-4 (109), and IL-13 (52) (Table 2).”
• The gut microbiota regulates bone mass in mice (2012, background): “Studies have shown that interleukin 1 (IL-1) is a downstream regulator of the effects of TNFa on inducing osteoclastogenesis and joint damage.((15,16)) The association between inflammation and bone loss is well established, and in autoimmune disease such as arthritis, osteoclastic bone resorption is”
• A crucial role for interleukin (IL)-1 in the induction of IL-17–producing T cells that mediate autoimmune encephalomyelitis (2006, positive): “This eff ect was dependent on IL-1, which is consistent with reports that TNF-α can promote IL-1 production and stromal cell IL-1RI expression (26) and that IL-1 was inhibited by treatment of psoriasis patients with a soluble TNF receptor (27).”
• Osteoclasts: what do they do and how do they do it? (2007, positive): “A major component of pathological bone loss as occurs in inflammatory osteolysis, reflects enhanced expression of RANKL and M-CSF induced by excess of local cytokines, particularly TNF.(40) Interestingly, TNFalso promotes c-fms production, and the osteolysis of the inflamed joint is completely arres”