Circulating myelinotoxic factors in human and experimental demyelinative disease.

T Yonezawa
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引用次数: 4

Abstract

Demyelinating agents in demyelinating diseases have been analysed using organoid cultures of the nervous tissue. The agents can be classified into humoral and cellular factors. Humoral factor is complement C3 dependent IgG antibody against glycolipids, such as galactocerebroside, sulfatide and ganglioside. Antigenicity of these glycolipids seems to be species specific. Other than rabbits, vulnerability seems to be low. Demyelinating pattern in vitro produced by application of antisera and patient sera are characterized by enhancement of activities of the macrophages. Adhesion of activated cells to myelin, penetration, loosening, splitting and vesicular dissolution of myelin lamellae are characteristic features. Hapten antigen described above also induces myelination inhibiting antibody, which interferes with in vitro myelination. Cellular factors are characterized by lymphotoxic effects and activation of macrophages. These alterations are identical to those by lymphokines liberated from T lymphocytes. Effects of humoral factors can be seen only in limited animal species, whereas cellular factors affect overall animals, suggesting the cellular factors play the major role in the processes of demyelination.

人类和实验性脱髓鞘疾病的循环髓鞘毒性因子。
利用神经组织的类器官培养分析了脱髓鞘疾病中的脱髓鞘药物。这些因子可分为体液因子和细胞因子。体液因子是补体C3依赖性IgG抗体,抗糖脂,如半乳糖脑苷、硫脂和神经节苷。这些糖脂的抗原性似乎是物种特异性的。除了兔子,其他动物的脆弱性似乎都很低。应用抗血清和患者血清产生体外脱髓鞘模式,其特征是巨噬细胞活性增强。活化细胞与髓磷脂的粘附、髓磷脂片的渗透、松动、分裂和囊状溶解是其特征。上述半抗原也诱导髓鞘形成抑制抗体,干扰体外髓鞘形成。细胞因子的特点是淋巴毒性作用和巨噬细胞的活化。这些改变与从T淋巴细胞中释放的淋巴因子的改变相同。体液因子的作用仅在有限的动物种类中可见,而细胞因子的作用则影响整个动物,提示细胞因子在脱髓鞘过程中起主要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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