Department of Pathology, Tufts University School of Medicine, Boston, MA 02111, USA.
J Immunol. 2010 Dec 15;185(12):7537-43. doi: 10.4049/jimmunol.1002173. Epub 2010 Nov 12.
We previously identified an enhancer element upstream of the mouse cd5 gene that was required in reporter assays for the induction of cd5 promoter activity by BCR cross-linking. This element is highly conserved in placental mammals. To determine its physiological role, we have now generated mice with a targeted deletion of the enhancer. The result is the loss of CD5 expression in peritoneal and splenic B-1a cells of adult mice and an inability to induce CD5 by cross-linking of the BCR on splenic B-2 cells. Surprisingly, CD5 expression on B-1a cells of neonatal mice was only minimally compromised. Cd5 enhancer deletion also had only a modest effect on CD5 expression in the T lineage. Thus, this enhancer provides age- and tissue-specific regulation of CD5 expression and is an example of the utilization of different modes of regulation of expression in T and B cells.
我们之前鉴定了一个位于小鼠 cd5 基因上游的增强子元件,该元件在 BCR 交联诱导 cd5 启动子活性的报告基因实验中是必需的。这个元件在胎盘哺乳动物中高度保守。为了确定其生理作用,我们现在生成了一个靶向缺失该增强子的小鼠。结果是成年小鼠腹膜腔和脾脏 B-1a 细胞中 CD5 表达的丧失,以及不能通过交联脾脏 B-2 细胞上的 BCR 来诱导 CD5。令人惊讶的是,新生小鼠 B-1a 细胞上的 CD5 表达仅受到轻微影响。Cd5 增强子缺失对 T 细胞谱系中 CD5 表达的影响也很小。因此,这个增强子提供了 CD5 表达的年龄和组织特异性调节,是 T 和 B 细胞中不同表达调控模式的一个例子。