Study of lymphocyte growth activity expressed on oligodendroglial membrane

我们分析了T淋巴细胞和最近建立的永生化神经胶质细胞系L3之间的细胞相互作用，L3保留了未成熟少突胶质细胞的几种特性（Aloisi等人，J Neurosci Res 27：16-24，1990）。L3少突胶质细胞（L3-OL）不能被诱导表达II类抗原，也不能特异性地将抗原呈递给同系特异性T淋巴细胞。然而，L3-OL强烈增强新鲜活化的白细胞介素-2（IL-2）依赖性T细胞和刀豆球蛋白A（ConA）活化的淋巴母细胞的增殖，无论其表面表型（CD 4+或CD 8+）的抗原特异性如何。在多聚甲醛固定的L3-OL细胞和膜制备物中观察到L3-OL的促有丝分裂作用，但在培养上清液中未观察到。无论是完整的L3-OL细胞，也没有直接的IL-2活性膜制剂。L3-OL细胞的促有丝分裂作用是由作为IL-2的共刺激因子的膜结构发挥的，这一结论得到了以下发现的支持：它在很大程度上被单克隆抗IL-2受体抗体阻断。这种作用不同于膜结合的IL-1、膜结合的肿瘤坏死因子-α、IL-3或IL-6，并且不能被这些细胞因子重建。

We analyzed cellular interactions between T lymphocytes and a recently established immortalized glial line, L3 that retains several properties of immature oligodendrocytes (Aloisi et al., J Neurosci Res 27 : 16-24, 1990). L3 oligodendrocytes (L3-OL) cannot be induced to express class II antigens, nor do they specifically present antigen to syngeneic specific T lymphocyte. However, L3-OL strongly enhance the proliferation of freshly activated, interleukin-2 (IL-2)-dependent T line lymphocytes and concanavalin A (ConA)-activated lymphoblasts, irrespective of their antigen specificity of surface phenotype (CD4+ or CD8+). The mitogen-ic effect of L3-OL was observed in paraformaldehyde-fixed L3-OL cells and in membrane preparations, but not in culture supernatant. Neither intact L3-OL cells nor membrane preparations had direct IL-2 activity. The conclusion that the mitogenic effect of L3-OL cells is exerted by membrane structures acting as a costimulatory factor(s) of IL-2 is supported by the finding that it is largely blocked by a monoclonal anti-IL-2 receptor antibody. The effect is distinct from membrane-bound IL-1, membrane-bound tumor necrosis factor-alpha, IL-3, or IL-6 and cannot be reconstituted by these cytokines.