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Sep 01, 2011
 |  BC Innovations  |  Cover Story

IL-20's osteoporosis connection

A group of Taiwanese researchers has shown that an antibody against IL-20 helped treat osteoporosis in mice.1 The findings have grabbed the attention of Novo Nordisk A/S, which has an anti-IL-20 mAb in Phase II testing to treat rheumatoid arthritis and is now considering exploring the bone loss indication.

IL-20, a member of the IL-10 family of proinflammatory cytokines, is expressed in monocytes, epithelial cells and endothelial cells. The team's previous studies showed that IL-20 was upregulated in mouse models of atherosclerosis2 and that an antibody against the cytokine reduced brain infarct size in mouse models of ischemic stroke.3

In 2006, the team showed that blocking IL-20 with a soluble form of its receptor, IL-20 receptor-a (IL20RA; IL20R1), decreased disease severity in mouse models of RA. Surprisingly, the therapeutic protected the animals against bone destruction as well.4 Those data led the team to speculate that IL-20 played a role in pathological bone loss and that inhibiting it could help treat osteoporosis.

In a new paper in The Journal of Experimental Medicine, the team has reported that serum levels of IL-20 were greater in patients with osteopenia (low bone mineral density) and osteoporosis than in healthy controls. Similar results were seen in mouse models of ovariectomy-induced osteoporosis.

Teasing out the mechanism, the group found that IL-20 regulated signaling between two proteins-tumor necrosis factor receptor superfamily member 11a (TNFRSF11A; RANK; CD265), which is expressed on osteoclasts, and receptor activator of NF-kB ligand...

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