Yamada A, Nikaido T, Nojima Y, Schlossman S F, Morimoto C
Division of Tumor Immunology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115.
J Immunol. 1991 Jan 1;146(1):53-6.
Fibronectin synergized with anti-CD3 antibody to promote CD4 cell proliferation in a serum-free culture system whereas no proliferation was observed when CD4 cells were cultured with anti-CD3 alone or fibronectin alone. In addition, anti-CD29 (integrin beta 1) as well as anti-VLA-5 (human fibronectin receptor) antibodies blocked this CD4 cell activation in this system. Although anti-CD3 alone or fibronectin alone cannot induce IL-2 message by CD4 cells, the combination of anti-CD3 plus fibronectin induced IL-2 message by CD4 cells. In an analysis of the molecular mechanism by which IL-2 message was generated, we showed that a fibronectin-VLA-5 fibronectin receptor interaction may contribute an independent signal distinct from the CD3 pathway of activation by the induction of an AP-1 transcriptional factor. Thus the VLA-5 fibronectin receptor on CD4 cells can play a complementary role in CD3-TCR-mediated signal transduction through its interaction with fibronectin.
在无血清培养体系中，纤连蛋白与抗CD3抗体协同作用，促进CD4细胞增殖；而单独用抗CD3或纤连蛋白培养CD4细胞时，未观察到增殖现象。此外，抗CD29（整合素β1）以及抗VLA-5（人纤连蛋白受体）抗体可阻断该体系中CD4细胞的激活。虽然单独的抗CD3或纤连蛋白不能诱导CD4细胞产生白细胞介素-2（IL-2）信息，但抗CD3与纤连蛋白的组合可诱导CD4细胞产生IL-2信息。在对IL-2信息产生的分子机制进行分析时，我们发现纤连蛋白-VLA-5纤连蛋白受体相互作用可能通过诱导AP-1转录因子，贡献一个不同于CD3激活途径的独立信号。因此，CD4细胞上的VLA-5纤连蛋白受体可通过与纤连蛋白相互作用，在CD3-TCR介导的信号转导中发挥互补作用。
