Grassi F, Lopalco L, Lanza P, Ciccomascolo F, Cazzola F, Di Martino A, Kirschner G, Callegaro L, Chieco-Bianchi L, Siccardi A G
Dipartimento di Biologia Genetica per le Scienze Mediche, Università di Milano, Italy.
Eur J Immunol. 1990 Jan;20(1):145-50. doi: 10.1002/eji.1830200121.
Human lymphocyte CD4 becomes undetectable in the presence of exogenous gangliosides (CD4 masking), as originally described by Offner et al. (J. Immunol. 1987. 139: 3295). CD4 masking is apparently due to in situ rearrangement of the glycoprotein; since no direct binding of ganglioside to CD4 could be demonstrated, it was suggested that the effect could be mediated by interactions with other, as yet unidentified, surface structures. To gain insight into the structural requirements of the interaction(s) that leads to CD4 masking, we assayed the effects of a battery of gangliosides and of ganglioside derivatives on (a) CD4 masking; (b) cholera toxin binding (as a well known ganglioside-protein interaction) and (c) inhibition of lymphocyte mitogenic proliferation (as a second ganglioside interaction with a lymphocyte surface target). Our results indicate that the three interactions are distinctly different, since ganglioside chemical groups which are essential for one of the interactions are irrelevant for the others, and lead to the conclusion that gangliosides can interact with lymphocyte surface targets in a number of ways, causing a number of independent biological effects.
如Offner等人最初所描述的（《免疫学杂志》，1987年，第139卷，第3295页），在存在外源性神经节苷脂的情况下，人类淋巴细胞CD4变得无法检测到（CD4掩盖）。CD4掩盖显然是由于糖蛋白的原位重排；由于未证明神经节苷脂与CD4有直接结合，因此有人提出这种效应可能是由与其他尚未确定的表面结构的相互作用介导的。为了深入了解导致CD4掩盖的相互作用的结构要求，我们检测了一系列神经节苷脂及其衍生物对（a）CD4掩盖；（b）霍乱毒素结合（作为一种众所周知的神经节苷脂-蛋白质相互作用）和（c）淋巴细胞有丝分裂增殖抑制（作为神经节苷脂与淋巴细胞表面靶点的第二种相互作用）的影响。我们的结果表明，这三种相互作用明显不同，因为对其中一种相互作用至关重要的神经节苷脂化学基团对其他相互作用无关紧要，并得出结论，神经节苷脂可以通过多种方式与淋巴细胞表面靶点相互作用，产生多种独立的生物学效应。
