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. 2015 Apr;135(4):1025-1032.
doi: 10.1038/jid.2014.532. Epub 2014 Dec 19.

IL-36γ (IL-1F9) is a biomarker for psoriasis skin lesions

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Free article

IL-36γ (IL-1F9) is a biomarker for psoriasis skin lesions

Angelo Massimiliano D'Erme et al. J Invest Dermatol. 2015 Apr.
Free article

Abstract

In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide. However, most of these markers are not only psoriasis-specific but also found in other inflammatory disorders. We performed an unsupervised cluster analysis of gene expression profiles in 150 psoriasis patients and other inflammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls). We identified a cluster of IL-17/tumor necrosis factor-α (TNFα)-associated genes specifically expressed in psoriasis, among which IL-36γ was the most outstanding marker. In subsequent immunohistological analyses, IL-36γ was confirmed to be expressed in psoriasis lesions only. IL-36γ peripheral blood serum levels were found to be closely associated with disease activity, and they decreased after anti-TNFα-treatment. Furthermore, IL-36γ immunohistochemistry was found to be a helpful marker in the histological differential diagnosis between psoriasis and eczema in diagnostically challenging cases. These features highlight IL-36γ as a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course. Furthermore, IL-36γ might also provide a future drug target, because of its potential amplifier role in TNFα- and IL-17 pathways in psoriatic skin inflammation.

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References

    1. J Immunol. 2011 Feb 15;186(4):2613-22 - PubMed
    1. Semin Immunol. 2013 Dec 15;25(6):458-65 - PubMed
    1. J Clin Invest. 2012 Nov;122(11):3965-76 - PubMed
    1. Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14863-8 - PubMed
    1. Nat Immunol. 2010 Nov;11(11):973 - PubMed

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