The IL-23/T17 pathogenic axis in psoriasis is amplified by keratinocyte responses

Michelle A. Lowes, Chris B. Russell, David A. Martin, Jennifer E. Towne, James G. Krueger

Research output: Contribution to journalReview articlepeer-review

371 Scopus citations


Psoriasis is a complex inflammatory process resulting from activation of the well-defined interleukin (IL)-23/T17 cytokine axis. We review the role of key cytokines IL-17 and IL-23 in psoriasis, as well as tumor necrosis factor (TNF)α, focusing on therapeutic cytokine interventions and what they reveal about psoriatic inflammation. The potential role of recently described epidermal IL-36RN and CARD14 genetic mutations in psoriasis pathogenesis is also explored, because they augment keratinocyte responses to proinflammatory cytokines. The discovery of these genetic mutations in familial and pustular psoriasis suggests new links between cytokine-induced gene products and IL-1 family members from keratinocytes, which may regulate features of the disease, including epidermal hyperplasia and neutrophil infiltrating responses.

Original languageEnglish (US)
Pages (from-to)174-181
Number of pages8
JournalTrends in Immunology
Issue number4
StatePublished - Apr 2013
Externally publishedYes


  • Anticytokine treatments
  • IL-23
  • Psoriasis
  • T cells
  • T17

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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