Constant remodelling of bones — up to 10% of the total mass every year — helps to maintain the optimal levels of calcium in the blood and also the structural function of the skeleton, but the identity of the molecules involved in controlling this process remains unclear. In April 18 Nature, Hiroshi Takayanagi and colleagues from University of Tokyo show that interferon-β (IFN-β) is pivotal in regulating bone homeostasis (Nature 2002, 416:744-749).

Takayanagi et al. observed that mice deficient in IFN-β exhibit severe loss of bone mass accompanied by enhanced osteoclastogenesis. Using this model they found that receptor activator of NF-κB ligand (RANKL) induced IFN-β in osteoclast precursor cells, and that IFN-β inhibited the differentiation by interfering with the RANKL-induced expression of c-Fos — a transcription factor essential for the formation of osteoclasts.

"This IFN-β gene induction is distinct from that induced by virus infections, and...

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