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首页> 外文期刊>Allergy >The IL IL ‐13/periostin/ IL IL ‐24 pathway causes epidermal barrier dysfunction in allergic skin inflammation
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The IL IL ‐13/periostin/ IL IL ‐24 pathway causes epidermal barrier dysfunction in allergic skin inflammation

机译：IL IL -13 / PERIOSTIN / IL IL -24途径会导致过敏性皮肤炎症中的表皮屏障功能障碍

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摘要

Abstract Background Barrier dysfunction is an important feature of atopic dermatitis ( AD ) in which IL ‐4 and IL ‐13, signature type 2 cytokines, are involved. Periostin, a matricellular protein induced by IL ‐4 or IL ‐13, plays a crucial role in the onset of allergic skin inflammation, including barrier dysfunction. However, it remains elusive how periostin causes barrier dysfunction downstream of the IL ‐13 signal. Methods We systematically identified periostin‐dependent expression profile using DNA microarrays. We then investigated whether IL ‐24 downregulates filaggrin expression downstream of the IL ‐13 signals and whether IL ‐13‐induced IL ‐24 expression and IL ‐24‐induced downregulation of filaggrin expression are dependent on the JAK / STAT pathway. To build on the significance of in vitro findings, we investigated expression of IL ‐24 and activation of STAT 3 in mite‐treated mice and in AD patients. Results We identified IL ‐24 as an IL ‐13‐induced molecule in a periostin‐dependent manner. Keratinocytes are the main IL ‐24‐producing tissue‐resident cells stimulated by IL ‐13 in a periostin‐dependent manner via STAT 6. IL ‐24 significantly downregulated filaggrin expression via STAT 3, contributing to barrier dysfunction downstream of the IL ‐13/periostin pathway. Wild‐type mite‐treated mice showed significantly enhanced expression of IL ‐24 and activation of STAT 3 in the epidermis, which disappeared in both STAT 6‐deficient and periostin‐deficient mice, suggesting that these events are downstream of both STAT 6 and periostin. Moreover, IL ‐24 expression was enhanced in the epidermis of skin tissues taken from AD patients. Conclusions The IL ‐13/periostin pathway induces IL ‐24 production in keratinocytes, playing an important role in barrier dysfunction in AD .
机译：摘要背景屏障功能障碍是特应性皮炎（AD）的重要特征，其中涉及IL-4和IL -13，签名型细胞因子。 PERIOSTIN，由IL -4或IL -13诱导的胰岛素蛋白在过敏性皮肤炎症的发作中起着至关重要的作用，包括阻隔功能障碍。然而，它仍然难以捉摸，脑蛋白是如何导致IL -13信号下游的屏障功能障碍。方法使用DNA微阵列系统地鉴定过肝素依赖性表达谱。然后研究IL -24是否向下调IL -13信号下游的叶虫蛋白表达以及IL -13诱导的IL -24表达和IL -24诱导的叶片表达的下调依赖于JAK / STAT途径。为了构建体外发现的重要性，我们研究了IL-24的表达和患有螨治疗小鼠和AD患者的STAT 3的活化。结果我们以紫外线依赖性方式鉴定为IL -13诱导的分子IL -24。异肌细胞是通过STAT 6. IL -24在近兴蛋白依赖性方式刺激的主要IL -24的组织居民细胞，通过Stat 6通过STAT 3显着下调的叶片表达，有助于IL -13下游的阻隔功能障碍/骨膜途径。野生型螨虫治疗小鼠显示出IL-24的显着增强，并在表皮中激活STAT 3，其在统计缺乏和肝胰岛素缺乏小鼠中消失，表明这些事件均为统计数据6和肝胰岛素的下游。此外，在来自AD患者的皮肤组织的表皮中增强了IL -24表达。结论IL -13 / PERIOSTIN途径在角蛋白细胞中诱导IL -24生产，在广告中的屏障功能障碍中发挥着重要作用。

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  • 来源
    《Allergy》 |2018年第9期|共11页
  • 作者

    Mitamura Y.; Nunomura S.; Nanri Y.; Ogawa M.; Yoshihara T.; Masuoka M.; Tsuji G.; Nakahara T.; Hashimoto‐Hachiya A.; Conway S. J.; Furue M.; Izuhara K.;

  • 作者单位

    Division of Medical BiochemistrySaga Medical SchoolSaga Japan;

    Division of Medical BiochemistrySaga Medical SchoolSaga Japan;

    Division of Medical BiochemistrySaga Medical SchoolSaga Japan;

    Division of Medical BiochemistrySaga Medical SchoolSaga Japan;

    Division of Medical BiochemistrySaga Medical SchoolSaga Japan;

    Division of Medical BiochemistrySaga Medical SchoolSaga Japan;

    Department of DermatologyKyushu UniversityFukuoka Japan;

    Department of DermatologyKyushu UniversityFukuoka Japan;

    Department of DermatologyKyushu UniversityFukuoka Japan;

    HB Wells Center for Pediatric ResearchIndiana University School of MedicineIndianapolis IN USA;

    Department of DermatologyKyushu UniversityFukuoka Japan;

    Division of Medical BiochemistrySaga Medical SchoolSaga Japan;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 医学免疫学;
  • 关键词

    atopic dermatitis; barrier dysfunction; IL ‐13; IL ‐24; periostin;

    机译：特应性皮炎;屏障功能障碍;IL -13;IL -24;PELIOSTIN;

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