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在受CD4影响的CD4+CD8+胸细胞中,对TCR表达的新型后翻译调节
J S Bonifacino1, S A McCarthy, J E Maguire
1Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892.
Nature
|March 15, 1990
概括
T细胞抗原受体 (TCR) 表面表达在发育过程中受到调节. 不成熟的胸细胞保留和降解TCR链,但抗CD4抗体治疗通过增强链从内细胞网膜逃脱来增加表面TCR.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 发展生物学 发展生物学
背景情况:
- 胸细胞上T细胞抗原受体 (TCR) 复杂表面表达对T细胞发育至关重要,并在分化过程中受到严格调节.
- 未成熟的胸细胞 (双阴性和双阳性) 表达较低水平的表面TCR,在成熟过程中显著增加到单个阳性阶段.
- 虽然TCR基因重组启动了表达,但在内部分化过程中控制定量表面TCR水平的机制在很大程度上是未知的.
研究的目的:
- 为了研究调节表皮细胞分化过程中表面T细胞抗原受体 (TCR) 表达量的定量变化的后翻译机制.
- 阐明抗CD4抗体治疗如何影响不成熟的胸细胞中的TCR表面表达水平.
- 为了确定RNA水平的变化,翻译或组合,或翻译后的过程,是否负责改变TCR表面表达.
主要方法:
- 对T细胞抗原受体 (TCR) 链保留和降解在胸细胞内质内网膜中的分析.
- 在体内对抗CD4抗体治疗的反应中,TCR表面表达的量化.
- 评估TCRRNA水平,翻译效率和与表面表达相关的组装状态.
主要成果:
- 不成熟的CD4 + CD8 + 胸细胞通常保留和降解超过90%的合成的T细胞抗原受体 (TCR) 链.
- 抗CD4抗体治疗显著增加了未成熟的CD4+CD8+胸细胞的表面TCR表达.
- 这种增长归因于新合成的TCR链从内细胞网膜中逃逸的增强,而不是改变的RNA水平,翻译或组装.
结论:
- 翻译后的机制,特别是细胞内膜网膜的保留和降解,对不成熟的胸细胞的T细胞抗原受体 (TCR) 复合体水平进行关键控制.
- 通过CD4表面分子发送信号可以调节这些翻译后调节机制,影响TCR表面表达.
- 了解这些调节途径是理解T细胞发育和潜在治疗干预措施的关键.
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