The immunopathogenesis of psoriasis

Dermatol Clin. 2015 Jan;33(1):13-23. doi: 10.1016/j.det.2014.09.002.


Psoriasis vulgaris is a chronic inflammatory skin disease that results from the complex interplay between keratinocytes, dendritic cells, and T cells. Keratinocytes trigger innate and adaptive immune responses. Dermal myeloid dendritic cells regulate T cell activation and production of cytokines and chemokines that amplify inflammation. Most of the psoriatic T cells discretely produce interferon-γ, interleukin (IL)-17, and IL-22. The initiation phase of psoriasis involves Toll-like receptors, antimicrobial peptide LL37, and plasmacytoid dendritic cells. Keratinocytes are the main cutaneous cell type expressing IL-17 receptors and hence the immune circuit is amplified by keratinocytes upregulating mRNAs for a range of inflammatory products.

Keywords: Dendritic cells; Immunology; Immunopathogenesis; Keratinocyte; Psoriasis; T cells.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adaptive Immunity
  • Animals
  • Dendritic Cells / immunology
  • Humans
  • Immunity, Innate
  • Interferon-gamma / immunology
  • Interleukin-17 / immunology
  • Keratinocytes / immunology
  • Killer Cells, Natural / immunology
  • Macrophages / immunology
  • Models, Biological
  • Neutrophils / immunology
  • Psoriasis / immunology*
  • Psoriasis / pathology
  • T-Lymphocytes / immunology*
  • Tumor Necrosis Factor-alpha / immunology


  • Interleukin-17
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma