Sunder-Plassmann R, Reinherz E L
Laboratory of Immunobiology, Dana-Farber Cancer Institute and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA.
J Biol Chem. 1998 Sep 11;273(37):24249-57. doi: 10.1074/jbc.273.37.24249.
The p56 Src family non-receptor tyrosine kinase has been shown to be critical for T lymphocyte differentiation and activation. Hence in the absence of p56, T cell receptor triggered activation does not occur. We now provide evidence for a CD2-based signaling pathway which, in contrast to that of the T cell receptor, is independent of p56. CD2-mediated interleukin-2 production occurs via activation of Jun kinase in cell lines lacking p56. Jun kinase then facilitates the binding of c-Jun/c-Fos heterodimers to the AP-1 consensus site and the subsequent transcriptional activity of the interleukin-2 promoter. These data elucidate differences between TCR and CD2 signaling pathways in the same T cells.
p56 Src家族非受体酪氨酸激酶已被证明对T淋巴细胞的分化和激活至关重要。因此,在缺乏p56的情况下,T细胞受体触发的激活不会发生。我们现在提供了基于CD2的信号通路的证据,与T细胞受体的信号通路不同,该通路独立于p56。在缺乏p56的细胞系中,CD2介导的白细胞介素-2产生是通过Jun激酶的激活而发生的。然后,Jun激酶促进c-Jun/c-Fos异二聚体与AP-1共有位点的结合以及白细胞介素-2启动子的后续转录活性。这些数据阐明了同一T细胞中TCR和CD2信号通路之间的差异。