通过B细胞中的抗原受体参与,保护Fas-依赖的Th1-介导的亡
T L Rothstein1, J K Wang, D J Panka
1Department of Medicine, Evans Memorial Department of Clinical Research, Boston University Medical Center, Massachusetts 02118.
Nature
|March 9, 1995
概括
激活的B细胞对T细胞诱导的死亡有不同的敏感性. 免疫球蛋白受体信号保护B细胞免受Fas介导的亡,确保抗原特异性细胞的存活.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 细胞灭亡 (apoptosis) 是一种死亡的过程.
背景情况:
- 细胞毒性CD4+ T辅助1 (Th1) 细胞通过一个Fas-依赖的途径诱导细胞亡.
- 活性B细胞是潜在的标,但它们对Th1-介导细胞毒性的敏感性尚未完全理解.
- B细胞刺激方法对Fas介导的亡敏感性的影响需要研究.
研究的目的:
- 调查B细胞刺激的模式是否会影响它们对由细胞毒性CD4+ Th1细胞诱导的Fas介导的亡的敏感性.
- 确定CD40连接体 (CD40L) 和抗免疫球蛋白M (抗IgM) 刺激在B细胞亡中的作用.
- 阐明B细胞耐药性或对T细胞中介细胞毒性的敏感性背后的机制.
主要方法:
- 与细胞毒性T细胞一起用CD40L和/或抗IgM刺激的B细胞共同培养.
- 使用Fas介导途径评估B细胞亡敏感性.
- 使用转基因B细胞 (3-83) 和具有特定MHCI类表达的细胞 (H-2Kk,H-2Kb,H-2Kd).
主要成果:
- CD40L刺激的B细胞对Fas介导的亡非常敏感.
- 抗IgM刺激的B细胞表现出对Fas介导的亡的抵抗力.
- 与CD40L和抗IgM联合刺激导致耐药性,这表明抗IgM介导的保护是主导和活跃的.
- 在与特定的MHC匹配脊髓细胞共同培养时,在转基因B细胞中也观察到抗药性.
结论:
- B细胞可以积极调节其自身被T细胞破坏.
- 免疫球蛋白受体的参与提供了对Fas-依赖性亡的保护.
- 这种保护作用于防故障机制,消除旁观者B细胞,同时确保抗原特异性B细胞的生存.
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