相关实验视频
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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
Published on: September 26, 2013
基碳化合物受体将TH17细胞介导的自身免疫与环境毒素联系起来
Marc Veldhoen1, Keiji Hirota, Astrid M Westendorf
1Division of Molecular Immunology, MRC National Institute for Medical Research, The Ridgeway, Mill Hill, London NW71AA, UK.
Nature
|March 26, 2008
概括
基碳化合物受体 (AHR) 调节T(H) 17细胞,在自身免疫性疾病中至关重要. AHR的激活增强了T(H) 17细胞的发育和IL-22的产生,可能会恶化自身免疫性疾病.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 毒理学 毒理学 毒理学
背景情况:
- 自身免疫性疾病正在增加,其中涉及T(H) 17细胞.
- 基碳化合物受体 (AHR) 是一种与二氧化毒性相关的转录因子.
- 环境因素可能会影响自身免疫性疾病的患病率.
研究的目的:
- 研究AHR在T(H) 17细胞发育和功能中的作用.
- 为了确定AHR激活是否影响自身免疫疾病模型.
主要方法:
- 在小鼠和人类T(H) 17细胞中检查了AHR表达.
- 在实验性自身免疫脑膜炎模型中使用了缺乏AHR的小鼠.
- 在AHR配体刺激时评估IL-22的产生和T(H) 17细胞的增殖.
主要成果:
- AHR在T(H) 17细胞中得到特定的表达,并促进IL-22的产生.
- 激活AHR可以增加T(H) 17细胞数量和细胞因子输出.
- 在野生型小鼠中,AHR激活会加剧实验性自身免疫脑膜炎.
结论:
- AHR在T(H) 17细胞生物学中发挥着重要作用.
- AHR配体可能在自身免疫性疾病的发病过程中起到辅助因素的作用.
- 准AHR可能为自身免疫性疾病提供治疗策略.
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