白细胞介素 33 由角质形成细胞中的肿瘤坏死因子-α和干扰素-γ诱导，并有助于过敏性接触性皮炎。
Interleukin 33 is induced by tumor necrosis factor alpha and interferon gamma in keratinocytes and contributes to allergic contact dermatitis.
机构信息
Department of Pediatrics, Faculty of Medicine, Saga University, Saga, Japan.
Community Medical Support Institute, Faculty of Medicine, Saga University, Saga, Japan.
出版信息
J Investig Allergol Clin Immunol. 2013;23(6):428-34.
BACKGROUND
Interleukin (IL) 33, a novel member of the IL-1 family, is produced mainly by epithelial cells and endothelial cells in response to various types of stress, including necrosis. The effects of IL-33 on the immune cells involved in allergic contact dermatitis have recently been revealed in vitro. However, in vivo, the induction mechanism and function of IL-33 are not fully understood.
OBJECTIVES
Our objectives were to investigate induction of IL-33 in keratinocytes and to evaluate the functions of IL-33 and its inducers in a murine model of allergic contact dermatitis.
MATERIAL AND METHODS
KERTr cells, a human keratinocyte cell line, were cultured with various cytokines, including tumor necrosis factor (TNF) alpha and interferon (IFN) gamma. IL-33 expression was detected using quantitative reverse transcriptase polymerase chain reaction, immunocytochemistry, and Western blotting. The functions of IL-33, TNF-a, and IFN-y in allergic contact dermatitis were evaluated using a murine model.
RESULTS
TNF-alpha and IFN-gamma induced expression of IL-33 mRNA and protein in KERTr cells. Blockade of IL-33 attenuated swelling in the ears of the experimental mice. Similar effects were noted for blockade of TNF-alpha and IFN-gamma in these mice.
CONCLUSIONS
TNF-alpha and IFN-gamma induce expression of IL-33, and IL-33 produced by keratinocytes contributes to allergic contact dermatitis. Blockade of IL-33, TNF-alpha, and IFN-gamma could represent novel and potent strategies to treat allergic contact dermatitis.
背景
白细胞介素 (IL) 33 是 IL-1 家族的新成员，主要由上皮细胞和内皮细胞在各种类型的应激下产生，包括坏死。IL-33 对涉及变应性接触性皮炎的免疫细胞的影响最近在体外得到了揭示。然而，在体内，IL-33 的诱导机制和功能尚未完全了解。
目的
我们的目的是研究角质形成细胞中 IL-33 的诱导，并评估 IL-33 及其诱导剂在变应性接触性皮炎小鼠模型中的功能。
材料和方法
培养人角质形成细胞系 KERTr 细胞与各种细胞因子，包括肿瘤坏死因子 (TNF)α 和干扰素 (IFN)γ。使用定量逆转录聚合酶链反应、免疫细胞化学和 Western blot 检测 IL-33 的表达。使用小鼠模型评估 IL-33、TNF-α 和 IFN-γ 在变应性接触性皮炎中的作用。
结果
TNF-α 和 IFN-γ 诱导 KERTr 细胞中 IL-33 mRNA 和蛋白的表达。阻断 IL-33 可减轻实验小鼠耳朵的肿胀。在这些小鼠中，阻断 TNF-α 和 IFN-γ 也有类似的作用。
结论
TNF-α 和 IFN-γ 诱导 IL-33 的表达，角质形成细胞产生的 IL-33 有助于变应性接触性皮炎。阻断 IL-33、TNF-α 和 IFN-γ 可能代表治疗变应性接触性皮炎的新的有效策略。
Zotero 插件