Wechsler D S, Kongshavn P A
Infect Immun. 1985 Jun;48(3):787-94. doi: 10.1128/iai.48.3.787-794.1985.
Plasma samples were collected from mice infected with Trypanosoma musculi at different times postinfection and administered to naive recipient mice either before or during T. musculi infection. The protective and curative activities of these plasma samples were shown to increase as the time of collection postinfection increased; plasma collected at 14 days postinfection was partially protective and partially curative, whereas that collected at 28 days postinfection was completely protective and curative. The curative activity was labile to heat treatment (30 min at 56 degrees C), whereas the protective activity was heat stable. Additional kinetic parameters relating to the efficacy of protection were investigated. Evidence is presented that both activities are immunoglobulin in nature. Protein A-Sepharose chromatography indicated that the activities are associated with the immunoglobulin G2a or immunoglobulin G3 subclasses of immunoglobulin G. The curative antibody appears to be intrinsically heat labile, since heat treatment of a purified immunoglobulin preparation abolished the ability to cure. Studies on the mechanism of parasite elimination from blood suggest that the process not only requires antibody but is also complement dependent.
在感染鼠锥虫后的不同时间点收集感染鼠的血浆样本,并在鼠锥虫感染前或感染期间将其给予未感染的受体小鼠。结果显示,这些血浆样本的保护和治疗活性随着感染后收集时间的增加而增强;感染后14天收集的血浆具有部分保护和部分治疗作用,而感染后28天收集的血浆则具有完全的保护和治疗作用。治疗活性对热处理(56℃ 30分钟)不稳定,而保护活性对热稳定。研究了与保护效果相关的其他动力学参数。有证据表明这两种活性本质上都是免疫球蛋白。蛋白A-琼脂糖层析表明,这些活性与免疫球蛋白G的免疫球蛋白G2a或免疫球蛋白G3亚类相关。治疗性抗体似乎本质上对热不稳定,因为纯化的免疫球蛋白制剂经热处理后丧失了治愈能力。关于从血液中清除寄生虫机制的研究表明,该过程不仅需要抗体,而且还依赖补体。