• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Clinical and experimental allergy : >CRTH2-dependent, STAT6-independent induction of cedar pollen dermatitis.
【24h】

CRTH2-dependent, STAT6-independent induction of cedar pollen dermatitis.

机译：Crth2依赖，毒蕈族花粉皮炎的独立诱导。

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

BACKGROUND: Airborne contact dermatitis to cedar pollen is a recently identified disease that generally affects individuals with cedar pollinosis of the nasal and/or ocular symptoms, as well as some patients with atopic dermatitis. OBJECTIVE: To elucidate the pathological mechanisms of cedar pollen dermatitis. METHODS: We established a mouse model of cedar pollen dermatitis by epicutaneous sensitization with Japanese cedar pollen antigen (Ag). RESULTS: Histologically, there was marked dermal cellular infiltrate, including eosinophils and mast cells, with epidermal thickening. The induction of dermatitis was accompanied by production of cedar pollen-specific IgE. In the lesional skin, IL-13, IL-18, eotaxin/chemokine (C-C motif) ligand (CCL) 11, regulated upon activation, normal T cell expressed and secreted/CCL5, macrophage-derived chemokine/CCL22 and thymus and activation-regulated chemokine/CCL17, but not IL-4 and IFN-gamma, were produced. Mast cell-deficient WBB6F1-W/W(v) mice failed to develop cedar pollen dermatitis, although regional lymph node cells proliferated in response to Cryptomeria japonica (Cry j) 1 and Cry j2 Ags in vitro. Surprisingly, the induction of dermatitis was independent of STAT6/IgE. In contrast, mice deficient in CRTH2, a receptor for prostaglandin D2 (PGD2), showed diminished inflammation. Consistent with this, ramatroban, a CRTH2 antagonist, significantly inhibited inflammatory cell infiltration. CONCLUSION: These data suggest that PGD2-CRTH2 signalling contributes to inflammation in cedar pollen dermatitis, and unlike cedar pollinosis of the nasal mucosa, STAT6 is not a therapeutic target for treatment.
机译：背景：空气传播的接触性皮炎至雪松花粉是最近鉴定的疾病，通常影响鼻腔和/或眼部症状的雪松花粉的个体，以及一些特应性皮炎的患者。目的：阐明雪松花粉皮炎的病理机制。方法：通过用日本雪松花粉抗原（AG），建立了雪松花粉皮炎的小鼠模型。结果：组织学上，具有明显的皮肤细胞浸润，包括嗜酸性粒细胞和肥大细胞，具有表皮增厚。皮炎诱导伴有雪松花粉特异性IgE的产生。在损伤皮肤，IL-13，IL-18，Eotaxin /趋化因子（CC基质）配体（CCl）11，调节在激活，正常的T细胞表达和分泌的/ CCl5，巨噬细胞衍生的趋化因子/ CCL22和胸腺和活化 - 制备了调节的趋化因子/ CCL17，但不是IL-4和IFN-Gamma。肥大细胞缺乏WBB6F1-W / W（V）小鼠未能开发雪松花粉皮炎，尽管响应Cryptomeria japonica（Cry J）1和体外Cry J2 AGS而增殖的区域淋巴结细胞。令人惊讶的是，皮炎的诱导与Stat6 / IgE无关。相反，缺乏在Crth2的小鼠，前列腺素D2（PGD2）的受体，显示出炎症枯萎病。符合此，Ramatroban是Crth2拮抗剂，显着抑制炎症细胞浸润。结论：这些数据表明，PGD2-CRTH2信号传导有助于雪松花粉皮炎中的炎症，与鼻粘膜的雪松花粉不同，STAT6不是治疗的治疗靶标。

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