在本位阶级切换和分化到肠膜内自身的IgA生成细胞
S Fagarasan1, K Kinoshita, M Muramatsu
1Department of Medical Chemistry, Graduate School of Medicine, Kyoto University, Yoshida Konoe-cho, Sakyo-ku, Kyoto, 606-8501, Japan.
Nature
|October 26, 2001
概括
肠膜自身产生免疫球蛋白A (IgA) 血细胞 in situ 从表达IgM的B细胞. 这个过程涉及类交换机重组 (CSR) 并发生在本地,挑战以前的迁移理论.
科学领域:
- 免疫学 免疫学 免疫学
- 胃肠病学 胃肠病学
- 细胞生物学 细胞生物学
背景情况:
- 肠道粘膜是关键的免疫屏障,免疫球蛋白A (IgA) 在管理与肠道微生物群和食抗原的相互作用方面发挥着关键作用.
- 传统的理解认为,产生IgA的细胞起源于皮耶尔斑块,并在抗原刺激后迁移到肠膜.
研究的目的:
- 为了研究肠道内自身的IgA产生细胞的起源和生成.
- 阐明激活诱导的细胞氨酸脱氨酶 (AID) 和类开关重组 (CSR) 在肠道IgA+细胞发育中的作用.
主要方法:
- 来自野生类型和缺乏AID的小鼠的B细胞的分析.
- 评估AID表达和圆形DNA转录在B细胞中.
- 在体外和体外培养实验中,采用自身B层和树皮细胞进行培养.
主要成果:
- 乳膜自身的IgA+B细胞表达了AID和CSR相关的转录,表明最近的类切换.
- 在自身膜中表达IgM的B细胞预先致力于IgA+分化.
- 与自身膜层细胞共同培养促进了IgA+血细胞与IgM+B细胞的分化.
结论:
- 肠膜自身中的IgA+血细胞是由B220+IgM+淋巴细胞局部生成的.
- 这种现场生成过程涉及正在进行的类交换机重组,该重组是在 lamina propria.
- 这些发现挑战了传统的IgA+细胞从肠外部位导向的模型.
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