科研之友
微信
新浪微博
Facebook
分享链接
摘要
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. The Journal of Immunology, 2010, 185: 7537-7543.
- 出版日期2010-12-15
