Grayson J M, Zajac A J, Altman J D, Ahmed R
Emory Vaccine Center and Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA 30322, USA.
J Immunol. 2000 Apr 15;164(8):3950-4. doi: 10.4049/jimmunol.164.8.3950.
Bcl-2 plays a critical role in regulating cell survival and apoptosis. We examined Bcl-2 expression in virus-specific CD8 T cells during the expansion, death, and memory phases of the T cell response following infection of mice with lymphocytic choriomeningitis virus (LCMV). Naive CD8 T cells expressed a basal level of Bcl-2 that was down-regulated in effector CD8 T cells just before the death phase. Bcl-2 levels remained low during the death phase but surviving memory CD8 T cells expressed higher levels of Bcl-2 than naive cells. These changes were shown to occur in LCMV TCR transgenic cells as well as virus-specific CD8 T cells in C57BL/6 and BALB/c mice identified by MHC class I tetramers. In all instances, memory CD8 T cells expressed higher levels of Bcl-2, suggesting that increased Bcl-2 expression plays a role in the long-term maintenance of memory CD8 T cells in vivo.
Bcl-2在调节细胞存活和凋亡过程中发挥着关键作用。我们检测了小鼠感染淋巴细胞性脉络丛脑膜炎病毒(LCMV)后,在T细胞反应的扩增、死亡和记忆阶段,病毒特异性CD8 T细胞中Bcl-2的表达情况。初始CD8 T细胞表达基础水平的Bcl-2,在死亡阶段前效应CD8 T细胞中该水平下调。在死亡阶段Bcl-2水平维持较低,但存活的记忆CD8 T细胞比初始细胞表达更高水平的Bcl-2。这些变化在LCMV TCR转基因细胞以及通过MHC I类四聚体鉴定的C57BL/6和BALB/c小鼠中的病毒特异性CD8 T细胞中均有出现。在所有情况下,记忆CD8 T细胞均表达更高水平的Bcl-2,这表明Bcl-2表达增加在体内记忆CD8 T细胞的长期维持中发挥作用。