KILLING OF RAT GLIAL-CELLS BY COMPLEMENT - DEFICIENCY OF THE RAT ANALOG OF CD59 IS THE CAUSE OF OLIGODENDROCYTE SUSCEPTIBILITY TO LYSIS
KILLING OF RAT GLIAL-CELLS BY COMPLEMENT - DEFICIENCY OF THE RAT ANALOG OF CD59 IS THE CAUSE OF OLIGODENDROCYTE SUSCEPTIBILITY TO LYSIS
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DOI：
10.1016/0165-5728(93)90189-6
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发表时间：
1993-11-01
影响因子：
3.3
通讯作者：
MORGAN, BP
中科院分区：
文献类型：
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作者：
PIDDLESDEN, SJ;MORGAN, BP
为了了解脱髓鞘疾病中补体介导的髓鞘/少突胶质细胞复合体损伤的机制，我们研究了培养的大鼠神经胶质细胞的溶解敏感性。已知大鼠少突胶质细胞对自体补体的溶解作用极其敏感，而相同培养系统中的其它细胞，包括衍生自相同祖细胞的II型星形胶质细胞，相对不敏感。在这里，我们证明了少突胶质细胞的补体敏感性与缺乏补体调节蛋白的表达，人CD 59的大鼠同源物，并且可以通过将纯化的大鼠CD 59掺入细胞膜来恢复补体抵抗。此外，补体抗性星形胶质细胞上的大鼠CD 59的中和作用使其易于裂解。未成熟的少突胶质细胞抵抗补体攻击，但不表达CD 59，这表明在少突胶质细胞成熟过程中，补体激活因子出现在膜上。
In an effort to understand the mechanisms of complement-mediated injury of the myelin/oligodendrocyte complex in demyelinating disease, we have examined the lytic susceptibility of rat glial cells in culture. It is known that rat oligodendrocytes are extremely sensitive to the lytic action of autologous complement, whereas other cells in the same culture system, including type II astrocytes which derive from the same progenitor cell, are relatively insensitive. Here we demonstrate that the complement sensitivity of oligodendrocytes is associated with a lack of expression of a complement-regulatory protein, the rat homologue of human CD59, and that complement resistance can be restored by the incorporation of purified rat CD59 into the cell membrane. Furthermore, neutralisation of rat CD59 on complement-resistant astrocytes renders them susceptible to lysis. Immature oligodendrocytes were resistant to complement attack yet did not express CD59, suggesting that a complement-activating factor appears on the membrane during oligodendrocyte maturation.