Department of Dermatology, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, China.
Department of Thoracic Surgery, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, China.
Cytokine. 2021 Feb;138:155391. doi: 10.1016/j.cyto.2020.155391. Epub 2020 Dec 8.
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.
银屑病是一种常见的慢性炎症性皮肤病,其中各种细胞因子起着有害的作用。细胞因子肿瘤坏死因子相关凋亡弱诱导剂(TWEAK)参与多种炎症性疾病的发病机制。然而,TWEAK 在银屑病的各种亚型中的潜在作用尚未深入研究。为了研究 TWEAK 的水平是否与临床特征以及一些已知的与银屑病相关的细胞因子(如白细胞介素(IL)-17A、IL-22、干扰素(IFN)-γ和 IL-36γ)的水平有关,我们招募了 20 名寻常型银屑病(PV)患者、8 名脓疱型银屑病(PP)患者、8 名红皮病型银屑病(EP)患者和 20 名健康对照者(HCs)纳入本研究。通过商业酶联免疫吸附试验试剂盒检测血清细胞因子水平。银屑病组 TWEAK、IL-17A、IL-22、IFN-γ 和 IL-36γ 的平均水平明显高于 HC 组。此外,在 PV 中 TWEAK 与 IL-17A/IFN-γ 之间,以及在 EP 中 TWEAK 与 IL-36γ 之间存在统计学显著相关性,但在任何亚型的银屑病中,TWEAK 与 IL-22 之间均无相关性。本研究表明,TWEAK 可能通过与 IL-17A、IFN-γ 或 IL-36γ 协同作用,而不是与 IL-22 协同作用,在 PV、PP 和 EP 的发病机制中发挥作用。