Skip to main navigation Skip to search Skip to main content

Involvement of the cytokine TWEAK in the pathogenesis of psoriasis vulgaris, pustular psoriasis, and erythrodermic psoriasis

  • Huixia Wang
  • , Sijia Wang
  • , Liang Li
  • , Xiuying Wang
  • , Chengfei Liu
  • , Mei Lu
  • , Yumin Xia
  • , Yale Liu
  • Xi'an Jiaotong University
  • Second Hospital of Shandong University

Research output: Contribution to journalArticlepeer-review

15 Scopus citations

Abstract

Psoriasis is a common chronic inflammatory dermatitis in which various cytokines play a detrimental role. The cytokine tumor necrosis factor-related weak inducer of apoptosis (TWEAK) is involved in the pathogenesis of multiple inflammatory disorders. However, the potential role of TWEAK in various subtypes of psoriasis has not been studied in depth. To investigate whether the levels of TWEAK are associated with clinical traits and the levels of some known psoriasis-related cytokines, such as interleukin (IL)-17A, IL-22, interferon (IFN)-γ, and IL-36γ, 20 patients with psoriasis vulgaris (PV), 8 patients with pustular psoriasis (PP), 8 patients with erythrodermic psoriasis (EP), and 20 healthy controls (HCs) were recruited into this study. The levels of serum cytokines were detected by commercial enzyme-linked immunosorbent assay kits. The average levels of TWEAK, IL-17A, IL-22, IFN-γ, and IL-36γ were significantly higher in the psoriasis groups than in the HC group. Furthermore, there was a statistically significant correlation between TWEAK and IL-17A/IFN-γ in PV and IL-36γ in EP, but there was no correlation between TWEAK and IL-22 in any subtype of psoriasis. This study suggests that TWEAK may have a role in the pathogenesis of PV, PP, and EP via synergy with IL-17A, IFN-γ, or IL-36γ, but not with IL-22.

Original languageEnglish
Article number155391
JournalCytokine
Volume138
DOIs
StatePublished - Feb 2021

Keywords

  • IFN-γ
  • IL-17A
  • IL-22
  • IL-36γ
  • Psoriasis
  • TWEAK

Fingerprint

Dive into the research topics of 'Involvement of the cytokine TWEAK in the pathogenesis of psoriasis vulgaris, pustular psoriasis, and erythrodermic psoriasis'. Together they form a unique fingerprint.

Cite this