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Uluckan et al. IL-17A causes local skin inflammation and accelerates bone loss


Psoriasis is associated with psoriatic arthritis in a proportion of patients, leading to bone loss and reduced bone formation. The impact on bone is mediated by interleukin 17A (IL-17A): Uluckan et al. now reveal that the degree of bone loss correlates closely with IL-17A levels in patients and in animal models.

They go on to uncover details of the molecular mechanisms involved. Although IL-17A was previously thought to be produced only by TH17 cells, other sources have been identified and this study confirms that several types of cell resident in the skin—namely innate lymphoid cells, keratinocytes and γδ T cells – all express IL-17A.

IL-17A produced in the skin acts locally but also systemically, inhibiting the Wnt signaling pathway in osteocytes and osteoblasts. In one mouse model, pharmacological blockade of IL-17A led to a recovery of mineral apposition, bone formation and bone mass. The authors conclude that IL-17A, produced in the skin, plays a critical role as a mediator of bone loss.

Editor’s comment: This study demonstrates that IL-17-mediated inflammatory skin diseases such as psoriasis cause suppression of bone formation by IL-17 via inhibition of Wnt signal in osteoblasts and osteocytes. Blocking the IL-17 signal may become a new therapeutic strategy in reducing bone loss associated with this type of inflammatory skin disease.

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