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白细胞介素 33 由银屑病角质形成细胞分泌,并通过角质形成细胞和肥大细胞的激活诱导促炎细胞因子。

IL-33 is secreted by psoriatic keratinocytes and induces pro-inflammatory cytokines via keratinocyte and mast cell activation.

出版信息

Exp Dermatol. 2012 Nov;21(11):892-4. doi: 10.1111/exd.12027.

Abstract

IL-33 is a novel pro-inflammatory cytokine and ligand for the orphan receptor ST2. Although originally defined as an inducer of Th2-mediated responses, IL-33 was recently found to be involved in arthritis, a Th1/Th17-mediated disease. Here, we assessed the ability of IL-33 to promote inflammation via mast cells (MCs) and keratinocytes (KCs) activation in psoriasis. IL-33 resulted elevated in the skin but not in the serum of psoriasis patients. IL-33 was secreted by psoriasis KCs and HaCaT cells after TNF-α stimulation. In HMC-1, TNF-α, but not IL-17, could induce a robust increase in IL-33 expression. In HaCaT cells, TNF-α was able to induce IL-6, MCP-1 and VEGF, and the addition of IL-33 reinforced these increases. TNF-α + IL-33 combination showed similar results in primary KCs and ex vivo skin organ culture. In conclusion, our study suggests that IL-33 may be involved in psoriasis biology via MCs and KCs.

摘要

IL-33 是一种新型促炎细胞因子,也是孤儿受体 ST2 的配体。虽然最初被定义为 Th2 介导反应的诱导剂,但最近发现 IL-33 参与了关节炎,这是一种 Th1/Th17 介导的疾病。在这里,我们评估了 IL-33 通过肥大细胞 (MCs) 和角质形成细胞 (KCs) 激活促进银屑病炎症的能力。IL-33 在银屑病患者的皮肤中而不是血清中升高。TNF-α 刺激后,银屑病 KCs 和 HaCaT 细胞分泌 IL-33。在 HMC-1 中,TNF-α 而非 IL-17 可诱导 IL-33 表达的强烈增加。在 HaCaT 细胞中,TNF-α 能够诱导 IL-6、MCP-1 和 VEGF,而添加 IL-33 则增强了这些增加。TNF-α+IL-33 组合在原代 KCs 和离体皮肤器官培养中也显示出相似的结果。总之,我们的研究表明,IL-33 可能通过 MCs 和 KCs 参与银屑病的生物学过程。

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