Voshol H, Dullens H F, Den Otter W, Vliegenthart J F
Utrecht University, Bijvoet Center, Dept. of Bio-Organic Chemistry, The Netherlands.
Anticancer Res. 1996 Jan-Feb;16(1):155-9.
Natural killer cells display spontaneous, non-MHC-restricted cytotoxicity against tumour cells, which is strongly enhanced after incubation with IL-2. The molecular background of the increased anti-tumour activity of these lymphokine-activated killer cells is still only partly understood.
In this paper, investigation has been made of the correlation between cell surface glycosylation and anti-tumour activity of LAK cells by stimulating peripheral blood lymphocytes with interleukin-2, in the presence of inhibitors of N- and O-glycosylation.
Inhibition of N- or O-glycosylation of proteins during IL-2 activation leads to a 70-80% decrease in the cytolytic activity of LAK cells against K562 and Daudi tumour cells, coinciding with drastic alterations in their cell surface carbohydrate profile.
The conclusion is drawn that there is a clear correlation between the glycosylation of LAK cell glycoproteins and their anti-tumour activity which points to the involvement of cell surface glycoconjugates in the development of LAK activity.
自然杀伤细胞对肿瘤细胞表现出自发的、非主要组织相容性复合体（MHC）限制的细胞毒性，在用白细胞介素-2（IL-2）孵育后，这种毒性会显著增强。这些淋巴因子激活的杀伤细胞抗肿瘤活性增加的分子背景仍仅部分为人所知。
本文通过在N-糖基化和O-糖基化抑制剂存在的情况下，用白细胞介素-2刺激外周血淋巴细胞，研究了LAK细胞的细胞表面糖基化与抗肿瘤活性之间的相关性。
在IL-2激活过程中抑制蛋白质的N-或O-糖基化会导致LAK细胞对K562和Daudi肿瘤细胞的细胞溶解活性降低70 - 80%，同时其细胞表面碳水化合物谱发生剧烈变化。
得出的结论是，LAK细胞糖蛋白的糖基化与其抗肿瘤活性之间存在明显的相关性，这表明细胞表面糖缀合物参与了LAK活性的发展。
