González-Cabrero J, Wise C J, Latchman Y, Freeman G J, Sharpe A H, Reiser H
Unidad de Investigación, Instituto de Investigaciones Médicas, Fundación Jiménez Díaz, Madrid 28040 Spain.
Proc Natl Acad Sci U S A. 1999 Feb 2;96(3):1019-23. doi: 10.1073/pnas.96.3.1019.
We have generated mice deficient in the expression of the lymphocyte cell surface antigen CD48 (Blast-1, BCM1, sgp-60) by gene targeting in embryonic stem cells. Mice homozygous for the CD48 mutation (CD48(-/-) mice) are severely impaired in CD4(+) T cell activation. Proliferative responses to mitogens, anti-CD3 mAb, and alloantigen are all reduced. Experiments in which T cells and antigen-presenting cells from either wild-type or CD48(-/-) mice were cocultured reveal that CD48 is important on both T cells and antigen-presenting cells. The most dramatic impairment was observed in experiments in which highly purified T cells were stimulated through the T cell receptor in the presence of the phorbol ester, phorbol 12-myristate 13-acetate. The results of these experiments raise the possibility that CD48 plays a role in signaling through the T cell receptor.
我们通过对胚胎干细胞进行基因靶向操作，培育出了淋巴细胞表面抗原CD48（Blast-1、BCM1、sgp-60）表达缺失的小鼠。CD48突变纯合子小鼠（CD48(-/-)小鼠）的CD4(+) T细胞活化严重受损。对丝裂原、抗CD3单克隆抗体和同种异体抗原的增殖反应均降低。将野生型或CD48(-/-)小鼠的T细胞与抗原呈递细胞共培养的实验表明，CD48在T细胞和抗原呈递细胞上均很重要。在使用佛波酯（佛波醇12-肉豆蔻酸酯13-乙酸酯）存在的情况下，通过T细胞受体刺激高度纯化的T细胞的实验中，观察到了最显著的损伤。这些实验结果增加了CD48在通过T细胞受体进行信号传导中发挥作用的可能性。
