Yoon Sang Soon, Kim Hyun Jung, Chung Doo Hyun, Kim Tae Jin
Department of Pathology, Center for Molecular Medicine, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon 440-746, Korea.
Mol Cells. 2004 Oct 31;18(2):186-91.
Although CD28 is the principal T cell costimulatory molecule for the T cell receptor, a number of other cell surface proteins have costimulatory functions and perform specific roles in different contexts. Here we analyzed the mechanism of CD99 costimulation of the T cell receptor. Cooperation of CD99 engagement with suboptimal TCR/CD3 signals resulted in greatly enhanced CD4+ T cell proliferation. CD99 costimulation also led to elevated expression of CD25 and GM1 on the CD4+ T cell surface within 3 days. In Jurkat TAg cells, CD99 costimulation led to increased apoptosis compared to stimulation with CD3 or CD99 alone. CD99 costimulation also augmented activation of MAP kinases, especially of JNK, and increased AP-1 activation was also observed using a luciferase reporter assay. These results show that CD99 has a costimulatory function for T cells and acts by a mechanism distinct from CD28.
尽管CD28是T细胞受体的主要T细胞共刺激分子，但许多其他细胞表面蛋白也具有共刺激功能，并在不同情况下发挥特定作用。在此，我们分析了CD99对T细胞受体共刺激的机制。CD99与次优TCR/CD3信号的协同作用导致CD4+T细胞增殖显著增强。CD99共刺激还导致3天内CD4+T细胞表面CD25和GM1表达升高。在Jurkat TAg细胞中，与单独用CD3或CD99刺激相比，CD99共刺激导致细胞凋亡增加。CD99共刺激还增强了丝裂原活化蛋白激酶（MAP激酶）的激活作用，尤其是JNK，并且使用荧光素酶报告基因检测也观察到AP-1激活增加。这些结果表明，CD99对T细胞具有共刺激功能，其作用机制不同于CD28。
