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Say it isn’t pso: IL-25 drives skin inflammation

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Science Immunology  04 May 2018:
Vol. 3, Issue 23, eaat9662
DOI: 10.1126/sciimmunol.aat9662

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  • IL-25 drives skin inflammation in psoriasis - the potential for clinical utility of IL-25 as a therapeutic target
    • Dr Dianne Sika-Paotonu, Associate Dean (Pacific)/Senior Lecturer Pathology & Molecular Medicine, Wellington School of Medicine & Health Sciences, University of Otago, New Zealand

    To the Editor,

    I read with interest the report prepared by Kalekbar, L.A., & Rosenblum, M.D., (1) and entitled: “Say it isn’t pso: IL-25 drives skin inflammation.” This commentary was based on work by Xu. et al (2) entitled: “An Interleukin-25-Mediated Autoregulatory Circuit in Keratinocytes Plays a Pivotal Role in Psoriatic Skin Inflammation.”

    Some of the key points highlighted were that IL-25 otherwise known as IL-17E and a cytokine belonging to the IL-17 family, is highly expressed in psoriasis (in humans and mice) and that intradermal IL-25 causes psoriasis-like disease in mice.

    In addition, IL-25 derived from keratinocytes was shown as being needed for the development of psoriasis-like disease and skin inflammation with treatment with anti-IL-25 able to improve disease. Collectively these results indicate that IL-17A expression during early psoriasis development triggers IL-25 expression and release from keratinocytes which acts in an autocrine manner and promotes keratinocyte proliferation, inducing pro-inflammatory responses via cytokines and chemokines mediated by STAT3 transcription factor activation.

    Although further work will be required, the potential clinical application of these findings remains promising. Psoriasis is a chronic inflammatory skin disease that continues to cause significant distress and discomfort to those suffering from the condition and the potential for clinical utility of IL-25 as a therapeutic target war...

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    Competing Interests: None declared.

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