Interleukin-25 fuels skin inflammation

A study of the role of interleukin-25 (IL-25) in psoriasis demonstrated the cytokine is involved in propelling skin inflammation in psoriasis, according to a recent analysis.

In the Editor’s Choice of the May 4 issue of Science Immunology, authors Lokesh Kalekar and Michael Rosenblum, Department of Dermatology, University of California, San Francisco, examined a recent study by Xu M, Lu H, Lee Y, et al. that was published in Immunity

Using a topical application of imiquimod in skin lesions of a mouse model of psoriasis, IL-25 expression was observed. Additionally, administering recombinant IL-25 intradermally fueled psoriasis-like disease in the mice.

“Expression of this cytokine is regulated by IL-17A, because IL-17A knockout mice have lower IL-25 expression in the imiquimod model,” Kalekar and Rosenblum wrote. “Imiquimod-induced disease was also substantially diminished in global IL-25 knockout mice.”

In mice with keratinocyte-selective deletion of the IL-25 gene, the pathology was weakened. A feedback loop of IL-17 receptor B with IL-25 resulted in keratinocyte proliferation and inflammatory gene expression in a STAT3-dependent manner. Further, treatment with anti-IL-25 improved disease expression.

“If these findings are validated in humans, inhibition of IL-25 may prove to be a novel therapeutic target in the treatment of psoriasis and associated diseases,” the authors wrote in the editorial.

The original study was published in the A study of the role of interleukin-25 (IL-25) in psoriasis demonstrated the cytokine is involved in propelling skin inflammation in psoriasis, according to a recent analysis.

In the Editor’s Choice of the May 4 issue of Science Immunology, authors Lokesh Kalekar and Michael Rosenblum, Department of Dermatology, University of California, San Francisco, examined a recent study by Xu M, Lu H, Lee Y, et al. that was published in Immunity.

Using a topical application of imiquimod in skin lesions of a mouse model of psoriasis, IL-25 expression was observed. Additionally, administering recombinant IL-25 intradermally fueled psoriasis-like disease in the mice.

“Expression of this cytokine is regulated by IL-17A, because IL-17A knockout mice have lower IL-25 expression in the imiquimod model,” Kalekar and Rosenblum wrote. “Imiquimod-induced disease was also substantially diminished in global IL-25 knockout mice.”

In mice with keratinocyte-selective deletion of the IL-25 gene, the pathology was weakened. A feedback loop of IL-17 receptor B with IL-25 resulted in keratinocyte proliferation and inflammatory gene expression in a STAT3-dependent manner. Further, treatment with anti-IL-25 improved disease expression.

“If these findings are validated in humans, inhibition of IL-25 may prove to be a novel therapeutic target in the treatment of psoriasis and associated diseases,” the authors wrote in the editorial.

The original study was published in the April 17 issue of Immunity.

*Study: https://www.cell.com/immunity/fulltext/S1074-7613(18)30116-X.

*Original source: http://immunology.sciencemag.org/content/3/23/eaat9662.full

https://www.cell.com/immunity/issue?pii=S1074-7613(17)X0008-3