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IL-30 ameliorates imiquimod and K14-VEGF induced psoriasis-like disease by inhibiting both innate and adaptive immunity disorders
Biochemical and Biophysical Research Communications ( IF 3.1 ) Pub Date : 2021-09-21 , DOI: 10.1016/j.bbrc.2021.09.042
Xiao Liu 1 , Zhonglan Hu 2 , Jun Zhang 3 , Teng Ma 3 , Wenlin Wu 3 , Xiaoqiong Wei 3 , Zhen Wang 3 , Huaping Zhen 3 , Hong Zhou 3 , Nongyu Huang 3 , Jiong Li 3
Affiliation  

Psoriasis is a severe skin disease with significant physical and psychological health consequences. As a typical type of immune disease, both innate and adaptive immunity disorders play key roles in the development of psoriasis. Interleukin (IL)-30 was thought as a natural antagonist of gp130-mediated signaling that affects T helper type 1 and 17 cell polarization by inhibiting IL-6 and IL-27 signaling pathways. Here, we found that, in vitro, IL-30 reduced cytokine levels of HaCaT keratinocytes and dendritic cells (DCs), weakened the maturationS of DCs, inhibited DC-mediated T cell proliferation, and blocked the activation of nuclear factor-κB. In vivo, IL-30 inhibited the development of skin disease in two animal models: Krt14-Vegfa and imiquimod (IMQ)-induced psoriasis-like skin disease. Thus, IL-30 may be useful as a therapeutic agent for controlling psoriasis.



中文翻译:

IL-30 通过抑制先天性和适应性免疫疾病来改善咪喹莫特和 K14-VEGF 诱导的银屑病样疾病

银屑病是一种严重的皮肤病,会对身体和心理健康造成严重影响。作为一种典型的免疫疾病,先天性和适应性免疫疾病在银屑病的发展过程中都起着关键作用。白细胞介素 (IL)-30 被认为是 gp130 介导的信号传导的天然拮抗剂,通过抑制 IL-6 和 IL-27 信号通路影响 T 辅助细胞 1 和 17 型细胞极化。在这里,我们发现,在体外,IL-30 降低了 HaCaT 角质形成细胞和树突细胞 (DC) 的细胞因子水平,削弱了 DC 的成熟,抑制了 DC 介导的 T 细胞增殖,并阻止了核因子-κB 的激活。在体内,IL-30 抑制了两种动物模型中皮肤病的发展:Krt14-Vegfa和咪喹莫特 (IMQ) 诱发的银屑病样皮肤病。因此,IL-30 可用作控制牛皮癣的治疗剂。

更新日期:2021-09-28
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