在B细胞中诱导人类IgE合成,由巨细胞和基细胞诱导
J F Gauchat1, S Henchoz, G Mazzei
1Glaxo Institute for Molecular Biology, Geneva, Switzerland.
Nature
|September 23, 1993
概括
乳腺细胞和基细胞是过敏的关键参与者,可以直接调节免疫球蛋白E (IgE) 的产生. 这些细胞表达CD40连接体 (CD40L),它刺激IgE合成,这表明,除了释放炎症媒介之外,还有一个新的作用.
科学领域:
- 免疫学 免疫学 免疫学
- 过敏研究 研究过敏
- 细胞生物学 细胞生物学
背景情况:
- 免疫球蛋白E (IgE) 与Fcepsilon R1结合在巨细胞和基细胞上,引发过敏反应.
- 过敏原对IgE的交联触发了炎症媒介的释放.
- 传统上,B细胞IgE的产生需要T细胞相互作用,粘附分子和IL-4和IL-13等细胞因子.
研究的目的:
- 研究巨细胞和基细胞在调节IgE产生中的作用.
- 为了确定巨细胞和基细胞能否提供IgE合成所需的细胞接触信号.
- 为了确定参与这个过程的特定分子.
主要方法:
- 使用的人类巨细胞 (HMC-1) 和基细胞 (KU812) 细胞系.
- 在IL-4的存在下评估IgE生产.
- 研究了CD40连接体 (CD40L) 的表达和功能.
- 检查了新鲜分离的人类肺部巨细胞和血液基细胞.
主要成果:
- 在IL-4的存在下,杆细胞和基细胞系为IgE合成提供细胞接触信号.
- 无论是HMC-1还是KU812细胞系都表达CD40L,CD40L被确定为诱导IgE生产的关键分子.
- 主要的人类巨细胞和基细胞也表达CD40L,并可以诱导IgE的产生.
结论:
- 乳腺细胞和基细胞可以独立于T细胞直接调节IgE的产生.
- 巨细胞和基细胞表达的CD40L在刺激IgE合成中起着至关重要的作用.
- 这些发现表明,在过敏性疾病中,巨细胞和基细胞的作用是双重的:媒介释放和IgE生产的直接调节.
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