• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Thymic stromal lymphopoietin-induced interleukin-17A is involved in the development of IgE-mediated atopic dermatitis-like skin lesions in mice
【24h】

Thymic stromal lymphopoietin-induced interleukin-17A is involved in the development of IgE-mediated atopic dermatitis-like skin lesions in mice

机译：胸腺基质淋巴细胞生成素诱导的白细胞介素17A参与小鼠IgE介导的特应性皮炎样皮肤病变的发展

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Atopic dermatitis (AD) is a chronic inflammatory skin disease associated with elevated levels of allergen-specific IgE. Although thymic stromal lymphopoietin (TSLP) and interleukin-17A (IL-17A) have been considered as important factors in allergic diseases, their relationships in AD have not been fully defined. Here, we show the contribution of TSLP-induced IL-17A responses to IgE-mediated AD-like skin lesions. BALB/c mice passively sensitized by intraperitoneal injections of ovalbumin (OVA)-specific IgE monoclonal antibody (mAb) were challenged with OVA applied to the skin six times. Treatment with anti-TSLP mAb during the second to sixth challenges inhibited IgE-mediated AD-like skin lesions and IL-17A production in lymph nodes. Furthermore, the increased number of IL-17A- producing CD4(+) and gamma delta T cells in lymph nodes and neutrophilic inflammation in the skin were reduced by anti-TSLP mAb. These findings prompted us to examine the roles of IL-17A. Treatment with anti-IL-17A mAb suppressed the AD-like skin lesions and neutrophilic inflammation; anti-Gr-1 mAb also inhibited them. Furthermore, treatment with CXCR2 antagonist reduced the AD-like skin lesions and neutrophilic inflammation accompanied by the reduction of IL-17A production; the increased CXCR2 expression in the epidermal cells was suppressed by anti-TSLP mAb. Meanwhile, these treatments, except for anti-Gr-1 mAb, inhibited the increased mast cell accumulation in the skin. Collectively, the mechanism of IgE mediating IL-17A-producing CD4(+) and gamma delta T cells through TSLP by repeated antigen challenges is involved in AD-like skin lesions associated with skin inflammation, such as neutrophil and mast cell accumulation; TSLP may regulate CXCR2 signalling-induced IL-17A production.
机译：特应性皮炎（AD）是一种与过敏原特异性IgE水平升高相关的慢性炎症性皮肤病。尽管胸腺基质淋巴细胞生成素（TSLP）和白介素17A（IL-17A）被认为是过敏性疾病的重要因素，但它们在AD中的关系尚未完全阐明。在这里，我们显示了TSLP诱导的IL-17A对IgE介导的AD样皮肤病的反应。通过腹膜内注射卵清蛋白（OVA）特异性IgE单克隆抗体（mAb）被动致敏的BALB / c小鼠，将OVA应用于皮肤六次。在第二至第六个挑战中，用抗TSLP单抗治疗可抑制IgE介导的AD样皮肤损伤和淋巴结中IL-17A的产生。此外，抗TSLP mAb减少了淋巴结中产生IL-17A的CD4（+）和γ-δT细胞的数量增加以及皮肤中的嗜中性炎症。这些发现促使我们检查了IL-17A的作用。抗IL-17A单抗治疗可抑制AD样皮肤损害和嗜中性粒细胞炎症。抗Gr-1 mAb也抑制了它们。此外，用CXCR2拮抗剂治疗可减少AD样皮肤损伤和嗜中性粒细胞炎症，并伴随IL-17A产生的减少。抗TSLP mAb抑制了表皮细胞中CXCR2表达的增加。同时，除抗Gr-1 mAb以外，这些治疗均能抑制肥大细胞在皮肤中积累的增加。总的来说，IgE通过反复的抗原攻击通过TSLP介导通过TSLP介导产生IL-17A的CD4（+）和伽马三角洲T细胞的机制涉及与皮肤炎症相关的AD样皮肤损害，例如中性粒细胞和肥大细胞的积累。 TSLP可能调节CXCR2信号传导诱导的IL-17A产生。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号