Effects of TNF-alpha inhibitors on circulating Th17 cells in patients affected by severe psoriasis

Drug Dev Res. 2014 Nov:75 Suppl 1:S73-6. doi: 10.1002/ddr.21202.

Abstract

Psoriasis was previously considered to be mostly a Th1 cell-related disorder, but Th17 cell has recently emerged as an important player in the pathogenesis of psoriasis. The Th17 immune pathway is increased in psoriatic patients, both in peripheral circulation and in skin lesions, and positively correlates with the Psoriasis Area and Severity Index. Anti-tumor necrosis factor alpha (TNF-α) agents, in addition to potent inhibition of TNF-α activity, are able to decrease IL-17 levels and Th17 cells in the skin and plasma of patients with moderate-to-severe psoriasis. We found a decrease in the median Th17 cell count in peripheral blood after 4 months' therapy with anti-TNF-α compared with baseline values, but the difference did not reach statistical significance, probably due to the small cohort size. Our data suggest that anti-TNF-α treatment for psoriasis is able to achieve a substantial Th17 cell count reduction in the peripheral blood of patients and that this decrease is significantly associated with an adequate response to biologic therapy, as previous studies in rheumatoid arthritis have shown.

Keywords: PASI; Th17; psoriasis; tumor necrosis factor (TNF) alpha inhibitors.

Publication types

  • Clinical Trial

MeSH terms

  • Adalimumab
  • Adult
  • Aged
  • Antibodies, Monoclonal, Humanized / pharmacology*
  • Antibodies, Monoclonal, Humanized / therapeutic use
  • Etanercept
  • Female
  • Humans
  • Immunoglobulin G / pharmacology*
  • Immunoglobulin G / therapeutic use
  • Lymphocyte Count
  • Male
  • Middle Aged
  • Psoriasis / blood
  • Psoriasis / drug therapy
  • Psoriasis / immunology*
  • Receptors, Tumor Necrosis Factor / therapeutic use
  • Severity of Illness Index
  • Th17 Cells / cytology
  • Th17 Cells / drug effects*
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*
  • Young Adult

Substances

  • Antibodies, Monoclonal, Humanized
  • Immunoglobulin G
  • Receptors, Tumor Necrosis Factor
  • Tumor Necrosis Factor-alpha
  • Adalimumab
  • Etanercept