IL-33 is secreted by psoriatic keratinocytes and induces pro-inflammatory cytokines via keratinocyte and mast cell activation
IL-33 is secreted by psoriatic keratinocytes and induces pro-inflammatory cytokines via keratinocyte and mast cell activation
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DOI：
10.1111/exd.12027
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发表时间：
2012-11-01
影响因子：
3.6
通讯作者：
Ayala, Fabio
中科院分区：
文献类型：
--
作者：
Balato, Anna;Lembo, Serena;Ayala, Fabio
IL-33 是一种新型促炎细胞因子和孤儿受体 ST2 的配体。尽管 IL-33 最初被定义为 Th2 介导反应的诱导剂，但最近发现 IL-33 与关节炎（一种 Th1/Th17 介导的疾病）有关。在这里，我们评估了 IL-33 在银屑病中通过肥大细胞 (MC) 和角质形成细胞 (KC) 激活促进炎症的能力。银屑病患者的皮肤中 IL-33 升高，但血清中未升高。 IL-33 由银屑病 KC 和 HaCaT 细胞在 TNF-α 刺激后分泌。在 HMC-1 中，TNF-α（而非 IL-17）可以诱导 IL-33 表达的强劲增加。在 HaCaT 细胞中，TNF-α 能够诱导 IL-6、MCP-1 和 VEGF，并且添加 IL-33 会增强这些增加。 TNF-α + IL-33 组合在原代 KC 和离体皮肤器官培养中显示出相似的结果。总之，我们的研究表明 IL-33 可能通过 MC 和 KC 参与银屑病生物学。
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-alpha stimulation. In HMC-1, TNF-alpha, but not IL-17, could induce a robust increase in IL-33 expression. In HaCaT cells, TNF-alpha was able to induce IL-6, MCP-1 and VEGF, and the addition of IL-33 reinforced these increases. TNF-alpha + 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.