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

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

细胞因子 TWEAK 参与寻常型银屑病、脓疱型银屑病和红皮病型银屑病的发病机制。

DOI:
10.1016/j.cyto.2020.155391
复制
发表时间:
2021-02-01
期刊:
影响因子:
3.8
通讯作者:
Liu, Yale
Liu, Yale
中科院分区:
医学3区
文献类型:
--
作者:
Wang, Huixia;Wang, Sijia;Liu, Yale

文献摘要

被引文献

相似文献

银屑病是一种常见的慢性炎症性皮炎,其中各种细胞因子起着有害作用。细胞因子肿瘤坏死因子相关凋亡弱诱导因子(TWEAK)参与多种炎症性疾病的发病机制。然而,TWEAK在银屑病各种亚型中的潜在作用尚未深入研究。为了探究TWEAK水平是否与临床特征以及一些已知的银屑病相关细胞因子如白细胞介素(IL)-17A、IL - 22、干扰素(IFN)-γ和IL - 36γ的水平相关,本研究招募了20例寻常型银屑病(PV)患者、8例脓疱型银屑病(PP)患者、8例红皮病型银屑病(EP)患者以及20例健康对照(HCs)。采用商品化的酶联免疫吸附测定试剂盒检测血清细胞因子水平。银屑病组中TWEAK、IL - 17A、IL - 22、IFN - γ和IL - 36γ的平均水平显著高于健康对照组。此外,在PV中TWEAK与IL - 17A/IFN - γ以及在EP中与IL - 36γ之间存在统计学显著相关性,但在任何银屑病亚型中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,在PV、PP和EP的发病机制中起作用。
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)-gamma, and IL-36 gamma, 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-gamma, and IL-36 gamma 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-gamma in PV and IL-36 gamma 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-gamma, or IL-36 gamma, but not with IL-22.