Mack David L, Leibowitz David S, Cooper Scott, Ramsey Heather, Broxmeyer Hal E, Hromas Robert
Department of Medicine, the Walther Oncology Center, Indiana University Medical Center, Indianapolis, IN 46202, USA.
Immunology. 2002 Dec;107(4):444-51. doi: 10.1046/j.1365-2567.2002.01523.x.
The haematopoietic homeobox gene Hex (also called Prh) is expressed in myeloid cells and B cells but not T cells. To investigate whether Hex levels might play a role in myeloid versus T-cell development, two types of transgenic mouse lines were constructed, each with ectopic expression of Hex in T cells (CD11a/Hex and Lck/Hex). Both these types of transgenic mouse had the same defects in T-cell maturation, indicating that proper T-cell development may be dependent not just on the up-regulation of lymphoid-specific transcriptional regulators but also on the co-ordinated down-regulation of myeloid-specific transcriptional regulators such as Hex. In addition, Hex over-expression significantly increased myeloid progenitor cycling, which may explain its role in retrovirally induced murine leukaemia.
造血同源框基因Hex(也称为Prh)在髓系细胞和B细胞中表达,但在T细胞中不表达。为了研究Hex水平是否可能在髓系与T细胞发育中发挥作用,构建了两种类型的转基因小鼠品系,每种品系的T细胞(CD11a/Hex和Lck/Hex)中均有Hex的异位表达。这两种类型的转基因小鼠在T细胞成熟方面都有相同的缺陷,表明正常的T细胞发育可能不仅依赖于淋巴特异性转录调节因子的上调,还依赖于髓系特异性转录调节因子(如Hex)的协同下调。此外,Hex的过表达显著增加了髓系祖细胞的循环,这可能解释了它在逆转录病毒诱导的小鼠白血病中的作用。