Pathophysiology of psoriasis: Recent advances on IL-23 and TH17 cytokines

Erin Fitch, Erin Harper, Iliyana Skorcheva, Stephen E. Kurtz, Andrew Blauvelt

Research output: Contribution to journalReview article

233 Scopus citations

Abstract

T helper (Th) 17 cells, a novel T-cell subset, have been implicated in the pathogenesis of psoriasis and other autoimmune inflammatory diseases. Interleukin (IL)-23 stimulates survival and proliferation of Th17 cells, and thus serves as a key master cytokine regulator for these diseases. In psoriasis, IL-23 is overproduced by dendritic cells and keratinocytes, and this cytokine stimulates Th17 cells within dermis to make IL-17A and 1L-22. IL-22, in particular, drives keratinocyte hyperproliferation in psoriasis. Future targeting of these key cytokines is likely to lead to dramatic clinical improvement in patients with psoriasis. This review focuses on the numerous recent studies on the roles of IL-23 and Th17 cells in the pathogenesis of psoriasis.

Original languageEnglish (US)
Pages (from-to)461-467
Number of pages7
JournalCurrent rheumatology reports
Volume9
Issue number6
DOIs
StatePublished - Dec 1 2007

ASJC Scopus subject areas

  • Rheumatology

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