Scanning the immunopathogenesis of psoriasis

Andrea Chiricozzi, Paolo Romanelli, Elisabetta Volpe, Giovanna Borsellino, Marco Romanelli

Research output: Contribution to journalReview articlepeer-review


Psoriasis is a chronic inflammatory skin disease, the immunologic model of which has been profoundly revised following recent advances in the understanding of its pathophysiology. In the current model, a crosstalk between keratinocytes, neutrophils, mast cells, T cells, and dendritic cells is thought to create inflammatory and pro-proliferative circuits mediated by chemokines and cytokines. Various triggers, including recently identified autoantigens, Toll-like receptor agonists, chemerin, and thymic stromal lymphopoietin may activate the pathogenic cascade resulting in enhanced production of pro-inflammatory and proliferation-inducing mediators such as interleukin (IL)-17, tumor necrosis factor (TNF)-α, IL-23, IL-22, interferon (IFN)-α, and IFN-γ by immune cells. Among these key cytokines lie therapeutic targets for currently approved antipsoriatic therapies. This review aims to provide a comprehensive overview on the immune-mediated mechanisms characterizing the current pathogenic model of psoriasis.

Original languageEnglish
Article number179
JournalInternational Journal of Molecular Sciences
Issue number1
Publication statusPublished - Jan 8 2018


  • Autoantigen
  • Autoreactive T cells
  • Chemokines
  • Cytokines
  • Dendritic cells
  • IL-17
  • IL-23
  • Immunology
  • Pathogenesis
  • Psoriasis

ASJC Scopus subject areas

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry


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