Mrkoci K, Kelm S, Crocker P R, Schauer R, Berger E G
Institute of Physiology, University of Zürich, Switzerland.
Glycoconj J. 1996 Aug;13(4):567-73. doi: 10.1007/BF00731444.
Previously, beta 1,3-galactosyltransferase-deficient (Tn+) and normal (TF+) T-lymphocyte clones have been established from a patient suffering from Tn-syndrome [Thurnher et al. (1992) Eur J Immunol 22: 1835-42]. Tn+ T lymphocytes express only Tn antigen GalNAc alpha 1-O-R) while other O-glycan structures such as sialosyl-Tn (Neu5Ac alpha 2,6GalNAc alpha 1-O-R) or TF (Gal beta 1-3GalNAc alpha 1-O-R) antigens are absent from these cells as shown by flow cytometry using specific mABs for TF and sialosyl-Tn antigen, respectively. Normal T lymphocytes express the TF antigen and derivatives thereof. The surface glycans of Tn+ and TF+ cells were then analysed by flow cytometry using the following sialic acid-binding lectins: Amaranthus caudatus (ACA), Maackia amurensis (MAA), Limax flavus (LFA), Sambucus nigra (SNA) and Triticum vulgare (WGA). Equal and weak binding of MAA and SNA to both TF+ and Tn+ cells was found. WGA, LFA and ACA bound more strongly to TF+ cells than to Tn+ cells. Binding of ACA to TF+ cells was enhanced after sialidase treatment. To investigate the possible biological consequences of hyposialylation, binding of three sialic acid-dependent adhesion molecules to Tn+ and TF+ cells was estimated using radiolabelled Fc-chimeras of sialoadhesin (Sn), myelin-associated glycoprotein (MAG) and CD22. Equal and strong binding of human CD22 to both TF+ and Tn+ cells was found. Whereas binding of Sn and MAG to TF+ cells was strong (100%), binding to Tn+ cells amounted only to 33% (Sn) and 19% (MAG). These results indicate that the in vivo interactions of T lymphocytes in the Tn syndrome with CD22 are not likely to be affected, whereas adhesion mediated by Sn or MAG could be strongly reduced.
此前，已从一名患有Tn综合征的患者体内建立了β1,3-半乳糖基转移酶缺陷型（Tn+）和正常（TF+）的T淋巴细胞克隆[图恩赫尔等人（1992年），《欧洲免疫学杂志》22: 1835 - 42]。Tn+ T淋巴细胞仅表达Tn抗原GalNAcα1 - O - R），而通过分别使用针对TF和唾液酸化Tn抗原的特异性单克隆抗体进行流式细胞术检测发现，这些细胞中不存在其他O - 聚糖结构，如唾液酸化Tn（Neu5Acα2,6GalNAcα1 - O - R）或TF（Galβ1 - 3GalNAcα1 - O - R）抗原。正常T淋巴细胞表达TF抗原及其衍生物。然后使用以下唾液酸结合凝集素通过流式细胞术分析Tn+和TF+细胞的表面聚糖：尾穗苋（ACA）、黑水缬草（MAA）、黄蛞蝓（LFA）、黑接骨木（SNA）和普通小麦（WGA）。发现MAA和SNA与TF+和Tn+细胞的结合相等且较弱。WGA、LFA和ACA与TF+细胞的结合比与Tn+细胞的结合更强。唾液酸酶处理后，ACA与TF+细胞的结合增强。为了研究低唾液酸化可能的生物学后果，使用唾液酸黏附素（Sn）、髓鞘相关糖蛋白（MAG）和CD22的放射性标记Fc嵌合体评估三种唾液酸依赖性黏附分子与Tn+和TF+细胞的结合。发现人CD22与TF+和Tn+细胞的结合相等且较强。而Sn和MAG与TF+细胞的结合较强（100%），与Tn+细胞的结合仅为33%（Sn）和19%（MAG）。这些结果表明，Tn综合征中T淋巴细胞在体内与CD22的相互作用不太可能受到影响，而由Sn或MAG介导的黏附可能会显著降低。
