Current Rheumatology Reports

, Volume 9, Issue 6, pp 461–467

Pathophysiology of psoriasis: Recent advances on IL-23 and Th17 cytokines

  • Erin Fitch
  • Erin Harper
  • Iliyana Skorcheva
  • Stephen E. Kurtz
  • Andrew Blauvelt
Article

DOI: 10.1007/s11926-007-0075-1

Cite this article as:
Fitch, E., Harper, E., Skorcheva, I. et al. Curr Rheumatol Rep (2007) 9: 461. doi:10.1007/s11926-007-0075-1

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 IL-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.

Copyright information

© Springer Science+Business Media, LLC 2007

Authors and Affiliations

  • Erin Fitch
  • Erin Harper
  • Iliyana Skorcheva
  • Stephen E. Kurtz
  • Andrew Blauvelt
    • 1
  1. 1.Dermatology ServiceVeterans Affairs Medical CenterPortlandUSA

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