The roles of cells and cytokines in the pathogenesis of psoriasis

Int J Dermatol. 2012 Apr;51(4):389-95; quiz 395-8. doi: 10.1111/j.1365-4632.2011.05154.x.

Abstract

Psoriasis is considered an immune chronic disease in which T cells are accepted as important. Nowadays, it is believed that psoriasis is most likely a T helper (Th)1/Th17 induced inflammatory disease. However, some other cells, such as endothelial cells, dendritic cells, monocytic cells, neutrophils, keratinocytes, and several cytokines, appear to have, at different stages of the disease, an important role in its pathogenesis. For instance, the response to psoriasis therapy is dependent not only on the inactivation of Th1 and Th17 immune responses but also on the inactivation of dendritic cell products. Moreover, interleukin (IL)-23 deregulation appears to be an independent factor in the pathogenesis of psoriasis. Indeed, currently, the IL-23/Th17 axis is believed to be crucial in psoriasis pathogenesis, and its inhibition appears to be important for therapeutic achievement. This review presents the roles and interactions of cells and cytokines that are related to psoriasis pathogenesis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Cytokines / metabolism*
  • Dendritic Cells / physiology
  • Humans
  • Immunologic Factors / therapeutic use
  • Interleukin-23 / metabolism
  • Lymphocyte Activation
  • Mast Cells / physiology
  • Neutrophils / physiology
  • Psoriasis / drug therapy
  • Psoriasis / immunology*
  • Psoriasis / metabolism
  • Th1 Cells / metabolism
  • Th17 Cells / metabolism
  • Th17 Cells / physiology
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors

Substances

  • Cytokines
  • Immunologic Factors
  • Interleukin-23
  • Tumor Necrosis Factor-alpha