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Pathogenesis and therapy of psoriasis

Nature volume 445, pages 866–873 (2007)Cite this article

Abstract

Psoriasis is one of the most common human skin diseases and is considered to have key genetic underpinnings. It is characterized by excessive growth and aberrant differentiation of keratinocytes, but is fully reversible with appropriate therapy. The trigger of the keratinocyte response is thought to be activation of the cellular immune system, with T cells, dendritic cells and various immune-related cytokines and chemokines implicated in pathogenesis. The newest therapies for psoriasis target its immune components and may predict potential treatments for other inflammatory human diseases.

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Figure 1: Histological components of a mature psoriatic plaque compared with normal skin.
Figure 2: A dynamic picture of the bidirectional flow of 'information' and cells in a mature psoriasis lesion: the yin and yang of psoriasis.
Figure 3: Potential cytokine networks in psoriatic lesions.
Figure 4: Effective treatments are available for psoriasis and reverse the disease phenotype.

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Acknowledgements

The authors and their primary research have been supported by grants from the NIH.

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  1. J.G.K. (jgk@rockefeller.edu). Reprints and permissions information is available at npg.nature.com/reprintsandpermissions.

Authors and Affiliations

  1. Laboratory for Investigative Dermatology, The Rockefeller University, 1230 York Avenue, Box 178, New York, New York 10021, USA.,

    Michelle A. Lowes & James G. Krueger

  2. Department of Genetics, Washington University, School of Medicine, 4566 Scott Avenue, Saint Louis, 63110, Missouri, USA

    Anne M. Bowcock

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Competing interests

James Krueger acknowledges research support from several companies (Genentech, Serono, Amgen, Biogen, Protein Design Lab and Bristol-Myers) that market biological drugs for psoriasis.

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Note added in proof: A recent study66 shows that IL-23 induces marked hyperplasia in epidermal keratinocytes in murine skin, and results suggest that this effect is mediated to a significant extent through IL-22 produced by TH17 T cells. However, keratinocyte hyperplasia is still present on an Il22-null background, which suggests that IL-23 or other factors independent of IL-22 also stimulate keratinocyte proliferation.

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Lowes, M., Bowcock, A. & Krueger, J. Pathogenesis and therapy of psoriasis. Nature 445, 866–873 (2007). https://doi.org/10.1038/nature05663

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