From bench to bedside--translational research in psoriasis

J Eur Acad Dermatol Venereol. 2010 Oct:24 Suppl 6:1-4. doi: 10.1111/j.1468-3083.2010.03829.x.

Abstract

For many years, psoriasis was firmly believed to be a disease of epidermal keratinocytes, but now is attributed to a combination of genetic and environmental factors that promote a T-cell mediated immune response in the skin. Psoriasis is now understood to be a systemic T-cell mediated autoimmune disease with the innate immune system playing an important role. Progress in understanding the pathogenesis of psoriasis has shown that following a stimulus, dendritic and T cell activation leads to the release of cytokines, chemokines and growth factors that initiate the proliferation and altered differentiation of keratinocytes. These factors subsequently lead to continuous activation of T cells and antigen-presenting cells, particularly dendritic cells, within the psoriatic plaque. This vicious cycle of psoriasis, in which the cytokines interleukin 12 (IL-12) and IL-23 play a pivotal role, is a logical target for biological therapy.

MeSH terms

  • Antibodies, Monoclonal / adverse effects
  • Antibodies, Monoclonal / therapeutic use*
  • Antibodies, Monoclonal, Humanized
  • Clinical Trials, Phase II as Topic
  • Clinical Trials, Phase III as Topic
  • Humans
  • Immunologic Factors / adverse effects
  • Immunologic Factors / therapeutic use*
  • Interleukin-12 / immunology
  • Interleukin-23 / immunology
  • Lymphocyte Activation
  • Psoriasis / immunology
  • Psoriasis / therapy*
  • Randomized Controlled Trials as Topic
  • Severity of Illness Index
  • T-Lymphocytes / immunology
  • Translational Research, Biomedical*
  • Treatment Outcome
  • Ustekinumab

Substances

  • Antibodies, Monoclonal
  • Antibodies, Monoclonal, Humanized
  • Immunologic Factors
  • Interleukin-23
  • Interleukin-12
  • briakinumab
  • Ustekinumab