Valenzuela A, Blanco J, Callebaut C, Jacotot E, Lluis C, Hovanessian A G, Franco R
Departament de Bioquímica i Biologia Molecular, Facultad de Química, Universidad de Barcelona, Spain.
Adv Exp Med Biol. 1997;421:185-92. doi: 10.1007/978-1-4757-9613-1_24.
CD26, known to be the adenosine deaminase (ADA) binding protein, has been implicated in HIV infection. In human B and T cell lines we show that, irrespective of CD4 expression, 125I-labeled ADA binding to CD26 is inhibited by recombinant soluble HIV-1 envelope glycoprotein gp120 and by HIV-1 infectious particles. Overlapping synthetic peptides covering the entire gp120 sequence were tested to map the region in gp120 responsible for ADA binding inhibition. Only peptides in the C3 region significantly inhibited the binding of ADA to CD26. These results indicate that a specific function of gp120 is the inhibition of ADA binding to CD26 in both CD4+ and CD4- cells. Since the interaction ecto-ADA/CD26 is required for the activation of T cells, it remains possible that HIV particle-mediated blockade of ecto-ADA/CD26 interaction may have significant consequences in the pathogenesis of AIDS disease.
CD26，已知为腺苷脱氨酶（ADA）结合蛋白，与HIV感染有关。在人B和T细胞系中，我们发现，无论CD4表达情况如何，重组可溶性HIV-1包膜糖蛋白gp120和HIV-1感染性颗粒均可抑制125I标记的ADA与CD26的结合。测试了覆盖整个gp120序列的重叠合成肽，以确定gp120中负责抑制ADA结合的区域。只有C3区域的肽能显著抑制ADA与CD26的结合。这些结果表明，gp120的一个特定功能是在CD4+和CD4-细胞中均抑制ADA与CD26的结合。由于细胞外ADA/CD26的相互作用是T细胞激活所必需的，因此HIV颗粒介导的细胞外ADA/CD26相互作用的阻断在艾滋病发病机制中可能具有重大影响。
