Scolding N J, Morgan B P, Compston D A
University of Cambridge Neurology Unit, Addenbrooke's Hospital, UK.
J Neuroimmunol. 1998 Apr 1;84(1):69-75. doi: 10.1016/s0165-5728(97)00241-5.
In multiple sclerosis, infiltrating T lymphocytes and perivascular microglia may initiate demyelinating lesions, but a role for antibody and complement in the ensuing inflammatory damage to myelin and oligodendrocytes is likely. In most tissues, ubiquitously expressed complement regulatory proteins prevent autologous destruction, protecting host cells from the powerful cytolytic activity of activated complement. We have studied the surface expression of a comprehensive range of complement regulatory proteins by live adult human oligodendrocytes in vitro. Only DAF of the activation pathway regulators was expressed, not CR1 or MCP. Of the membrane attack pathway regulatory proteins, HRF was not expressed, while substantial heterogeneity of CD59 expression by oligodendrocytes was found. Clusterin expression was not found. A relative deficiency of protective complement regulatory proteins on human oligodendrocytes may contribute to their selective damage in multiple sclerosis.
在多发性硬化症中，浸润的T淋巴细胞和血管周围小胶质细胞可能引发脱髓鞘病变，但抗体和补体在随后对髓鞘和少突胶质细胞的炎性损伤中可能起作用。在大多数组织中，普遍表达的补体调节蛋白可防止自身破坏，保护宿主细胞免受活化补体强大的细胞溶解活性的影响。我们在体外研究了成年活人少突胶质细胞表面一系列补体调节蛋白的表达情况。激活途径调节蛋白中只有衰变加速因子（DAF）表达，而补体受体1（CR1）或膜辅蛋白（MCP）未表达。在膜攻击途径调节蛋白中，同源限制因子（HRF）未表达，而发现少突胶质细胞的CD59表达存在显著异质性。未发现簇集素表达。人类少突胶质细胞上保护性补体调节蛋白的相对缺乏可能导致它们在多发性硬化症中受到选择性损伤。
