TNF-alpha and apoptosis: implications for the pathogenesis and treatment of psoriasis

J Drugs Dermatol. 2002 Dec;1(3):264-75.


TNF-alpha is a key cytokine in innate immune responses and is increased in psoriatic lesions. TNF-alpha has many effects, ranging from inflammation to apoptosis. These effects are reviewed to better understand the role of TNF-alpha as it relates to the pathogenesis and treatment of psoriasis. TNF-alpha increases production of pro-inflammatory molecules (e.g. IL-1, IL-6, IL-8, NF-kappa B, vasoactive intestinal peptide) and adhesion molecules (e.g. intercellular adhesion molecule-1, P-selectin, E-selectin). TNF-alpha promotes apoptosis through binding to the TNF-receptor 1; however, psoriatic lesions are hyperproliferative despite an increase in TNF-alpha. This paradox is partially explained as NF-kappa B activation seems to inhibit TNF-alpha-induced apoptosis. The importance of TNF-alpha and apoptosis in psoriasis is shown through the review of clinical trials using anti-TNF-alpha immunobiologics (e.g. etanercept, infliximab) and apoptosis-inducing treatments that result in clinical improvement of the disease.

Publication types

  • Review

MeSH terms

  • Apoptosis / physiology*
  • Humans
  • Psoriasis* / drug therapy
  • Psoriasis* / etiology
  • Randomized Controlled Trials as Topic
  • Tumor Necrosis Factor-alpha* / metabolism
  • Tumor Necrosis Factor-alpha* / physiology
  • Tumor Necrosis Factor-alpha* / therapeutic use


  • Tumor Necrosis Factor-alpha