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Bone destroying cells (red) flourish in the presence (top) of the IL-17 cytokine.
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T cells that produce cytokine IL-17 activate bone-destroying osteoclasts, report Sato et al. on page 2673. The finding pinpoints a potentially powerful target for autoimmine arthritis therapy.
Autoimmune arthritis, such as rheumatoid arthritis, is a T cell–driven disease, in which bones are destroyed by hyperactive bone-resorbing osteoclasts. Activated T cells have long been implicated in arthritic inflammation and the resulting bone destruction, but exactly which type of T cell is responsible has never been confirmed. T helper (Th)-1 cells, the cells that promote cellular immunity, have received the lion's share of the blame. Yet Th1's signature cytokine, IFN
, actually inhibits bone resorption by osteoclasts.
The study by Sato et al. helps resolve this paradox by putting the blame for inflammatory bone destruction on a recently described T cell subset called Th17. Th17 cells, named for their propensity to secrete the cytokine IL-17, have also been implicated in other models of autoimmune inflammation.
The team tested whether various T cell subsets—Th17, Th1, Th2, and regulatory T cells—affected osteoclasts. They found that only Th17 cells enhanced osteoclast differentiation—a prerequisite for bone resorption. IL-17 itself also promoted osteoclast differentiation. The induction of osteoclast differentiation was only seen when bone-forming osteoblast cells were also present in the culture. Osteoblasts provide osteoclasts with differentiation signals; thus it now appears that IL-17 might prompt the osteoblasts to release these signals.
Current treatments for autoimmune arthritis reduce inflammation by using broad-based immunosuppression. The identification of both the specific T cell subset and the cytokine responsible for promoting bone resorption might lead to a more powerful therapy that also targets skeletal damage. 
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