Mamalaki C, Tanaka Y, Corbella P, Chandler P, Simpson E, Kioussis D
Laboratory of Molecular Immunology, National Institute for Medical Research, London, UK.
Int Immunol. 1993 Oct;5(10):1285-92. doi: 10.1093/intimm/5.10.1285.
Exposure of mice transgenic for a TCR (F5) to cognate peptide antigen results in thymic depletion of CD4+CD8+ cells and expansion and activation of peripheral CD8+ TCR(tg)+ T cells. In the thymus apoptotic DNA ladder is evident as early as 3 h after peptide injection. Long exposure of intact or thymectomized F5 TCR transgenic mice to peptide antigen leads to depletion of most of the peripheral CD8+ T cells bearing the F5 receptor, with the remaining cells having lower levels of transgenic TCR compared with non-treated animals. In the thymus of intact F5 TCR transgenic mice such continuous exposure to antigen results in the reappearance of CD4+CD8+ with lower levels of the transgenic receptor.
将携带TCR(F5)的转基因小鼠暴露于同源肽抗原会导致胸腺中CD4+CD8+细胞耗竭,以及外周CD8+ TCR(tg)+ T细胞扩增和活化。在胸腺中,早在注射肽后3小时就可明显观察到凋亡DNA梯带。完整或胸腺切除的F5 TCR转基因小鼠长期暴露于肽抗原会导致大多数携带F5受体的外周CD8+ T细胞耗竭,与未处理动物相比,剩余细胞的转基因TCR水平较低。在完整的F5 TCR转基因小鼠胸腺中,这种持续暴露于抗原会导致转基因受体水平较低的CD4+CD8+细胞重新出现。