McDermott J R, Keith A B
Acta Neurol Scand. 1979 Sep;60(3):140-8. doi: 10.1111/j.1600-0404.1979.tb02961.x.
This study confirms previous reports that myelin basic protein loses its encephalitogenic activity when incubated in normal serum at 37 degrees C. The mechanisms for this was studied. 125I-labelled human myelin basic protein was rapidly degraded by normal guinea pig serum to low molecular weight products as shown by polyacrylamide gel electrophoresis. An intermediate product of molecular weight about 6000 daltons was seen. Plasma had a much lower degradative activity than serum; the half life of myelin basic protein was 3.8 hours in plasma compared with 12 minutes in serum. Serum degraded myelin basic protein was no longer capable of suppressing experimental allergic encephalomyelitis in the guinea pig nor of eliciting delayed-type hypersensitivity in guinea pigs sensitized to myelin basic protein.
本研究证实了先前的报道,即髓鞘碱性蛋白在37℃于正常血清中孵育时会丧失其致脑炎活性。对其机制进行了研究。如聚丙烯酰胺凝胶电泳所示,正常豚鼠血清可将125I标记的人髓鞘碱性蛋白迅速降解为低分子量产物。可见一种分子量约为6000道尔顿的中间产物。血浆的降解活性远低于血清;髓鞘碱性蛋白在血浆中的半衰期为3.8小时,而在血清中为12分钟。血清降解的髓鞘碱性蛋白不再能够抑制豚鼠实验性过敏性脑脊髓炎,也不能在对髓鞘碱性蛋白致敏的豚鼠中引发迟发型超敏反应。