2. Academic Validation
  3. IL-23 stimulates epidermal hyperplasia via TNF and IL-20R2-dependent mechanisms with implications for psoriasis pathogenesis

IL-23 stimulates epidermal hyperplasia via TNF and IL-20R2-dependent mechanisms with implications for psoriasis pathogenesis

  • J Exp Med. 2006 Nov 27;203(12):2577-87. doi: 10.1084/jem.20060244.
Jason R Chan 1,  Wendy Blumenschein,  Erin Murphy,  Caroline Diveu,  Maria Wiekowski,  Susan Abbondanzo,  Linda Lucian,  Richard Geissler,  Scott Brodie,  Alexa B Kimball,  Daniel M Gorman,  Kathleen Smith,  Rene de Waal Malefyt,  Robert A Kastelein,  Terrill K McClanahan,  Edward P Bowman
Affiliations

Affiliation

  • 1 Discovery Research, Schering-Plough Biopharma (formerly DNAX Research, Inc.), Palo Alto, CA 94304, USA.
PMID: 17074928 DOI: 10.1084/jem.20060244
Abstract

Aberrant cytokine expression has been proposed as an underlying cause of psoriasis, although it is unclear which cytokines play critical roles. Interleukin (IL)-23 is expressed in human psoriasis and may be a master regulator cytokine. Direct intradermal administration of IL-23 in mouse skin, but not IL-12, initiates a tumor necrosis factor-dependent, but IL-17A-independent, cascade of events resulting in erythema, mixed dermal infiltrate, and epidermal hyperplasia associated with parakeratosis. IL-23 induced IL-19 and IL-24 expression in mouse skin, and both genes were also elevated in human psoriasis. IL-23-dependent epidermal hyperplasia was observed in IL-19-/- and IL-24-/- mice, but was inhibited in IL-20R2-/- mice. These data implicate IL-23 in the pathogenesis of psoriasis and support IL-20R2 as a novel therapeutic target.

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