Mechanisms of protective immunity against Schistosoma mansoni infection in mice vaccinated with irradiated cercariae. II. Analysis of immunity in hosts deficient in T lymphocytes, B lymphocytes, or complement.
Mechanisms of protective immunity against Schistosoma mansoni infection in mice vaccinated with irradiated cercariae. II. Analysis of immunity in hosts deficient in T lymphocytes, B lymphocytes, or complement.
复制标题
接种辐照尾蚴的小鼠抗曼氏血吸虫感染的保护性免疫机制。
作者：
A. Sher;S. Hieny;S. James;R. Asofsky
用辐照曼氏血吸虫尾蚴免疫遗传性或诱导性免疫缺陷的实验小鼠，4周后测定其对攻击感染的抵抗力。无胸腺裸鼠未能开发免疫挑战或可检测到的抗体反应，而杂合子（nu/+）的控制和胸腺移植物的裸鼠表现出高度显着的抵抗力和抗幼稚体抗体水平。同样，在出生时注射抗μ链抗血清导致B淋巴细胞缺陷的接种小鼠中未观察到抗性或抗体产生。相反，在补体第五组分（C5）遗传缺陷的小鼠和在用眼镜蛇毒因子处理的攻击前去补体的小鼠中观察到正常水平的疫苗诱导的抗性。这些结果表明，辐照尾蚴诱导的对攻击感染的抵抗力是胸腺和B淋巴细胞依赖的，因此可能是针对寄生蠕虫的特异性免疫应答的结果。这些数据还反对补体在疫苗诱导免疫的效应机制中的作用。
Laboratory mice with genetic or induced immunodeficiencies were vaccinated with irradiated cercariae of Schistosoma mansoni and assayed 4 wk later for their resistance to challenge infection. Athymic nude mice failed to develop immunity to challenge or detectable antibody responses to schistosomula, whereas heterozygote (nu/+) controls and nude mice with thymus grafts displayed highly significant levels of resistance and anti-schistosomulum antibody. Similarly, no resistance or antibody production as observed in vaccinated mice that had been made deficient in B lymphocytes by the injection of anti-mu-chain antisera from birth. In contrast, normal levels of vaccine-induced resistance were observed in mice genetically deficient in the fifth component of complement (C5) and in mice decomplemented before challenge by treatment with cobra venom factor. These results indicate that the resistance to challenge infection induced by irradiated cercariae is both thymus and B lymphocyte dependent and therefore is likely to result from specific immune responses directed against schistosome worms. The data also argue against a role for complement in the effector mechanism of vaccine-induced immunity.