Correa-Oliveira R, Sher A, James S L
J Immunol. 1984 Sep;133(3):1581-6.
Inbred P4 strain mice have previously been shown to be uniquely defective in their resistance to challenge infection induced by irradiated cercariae of Schistosoma mansoni. To assess whether the low levels of resistance developed by vaccinated P mice could be due to a defective antibody response, we compared the anti-schistosomulum antibody responses in vaccinated P animals with those occurring in vaccinated C57BL/6J (B6) mice, a strain that consistently develops high levels of resistance to challenge infection. Our results indicate that vaccinated P mice develop levels of total anti-schistosomulum antibodies that are significantly lower than those occurring in B6 mice for at least 15 wk after immunization, with the exception of the fifth week, at which time the responses are indistinguishable. Further analysis revealed that the defect in P strain antibody response occurs specifically in the IgM isotype and that specific IgM levels in P mice are less than one-half the levels in B6 mice at every time point examined. In contrast, no differences in total IgM immunoglobulins were evident when sera from normal (nonvaccinated) P and B6 mice were compared. P mouse anti-schistosomulum IgG antibody responses reached the same levels as those observed in B6 mice by 5 wk after vaccination. However, a much faster decay in IgG antibody levels occurred after this time point in P animals. No differences were observed when the levels of anti-schistosomulum antibodies occurring in each of the major IgG isotypes (IgG1, IgG2a, IgG2b, IgG3) were compared in sera from P and B6 mice vaccinated 4 wk previously. Similarly, vaccinated P and B6 mice were found to mount indistinguishable IgG anamnestic responses after challenge infection. Finally, no differences between vaccinated P and B6 mice were observed when immediate (30 min) skin test and mast cell degranulation responses to a soluble schistosome antigenic preparation were compared. The above findings suggest that P strain mice have a specific defect in their ability to mount IgM antibody responses after immunization with irradiated cercariae. The possible contribution of this defect in IgM response to the decreased resistance of vaccinated P mice to challenge infection is discussed.
近交系P4小鼠先前已被证明在抵抗曼氏血吸虫辐照尾蚴诱导的攻击感染方面存在独特缺陷。为了评估接种疫苗的P小鼠产生的低水平抵抗力是否可能归因于抗体反应缺陷，我们比较了接种疫苗的P动物与接种疫苗的C57BL/6J（B6）小鼠的抗血吸虫童虫抗体反应，C57BL/6J小鼠是一种对攻击感染始终产生高水平抵抗力的品系。我们的结果表明，接种疫苗的P小鼠产生的总抗血吸虫童虫抗体水平在免疫后至少15周内显著低于B6小鼠，第五周除外，此时两者反应无差异。进一步分析表明，P品系抗体反应缺陷 specifically发生在IgM同种型中，并且在每个检测时间点，P小鼠的特异性IgM水平不到B6小鼠的一半。相比之下，比较正常（未接种疫苗）的P和B6小鼠的血清时，总IgM免疫球蛋白没有明显差异。接种疫苗后5周，P小鼠的抗血吸虫童虫IgG抗体反应达到与B6小鼠相同的水平。然而，在此时间点之后，P动物的IgG抗体水平下降得更快。比较4周前接种疫苗的P和B6小鼠血清中各主要IgG同种型（IgG1、IgG2a、IgG2b、IgG3）的抗血吸虫童虫抗体水平时，未观察到差异。同样，在攻击感染后，接种疫苗的P和B6小鼠产生的IgG回忆反应无差异。最后，比较接种疫苗的P和B6小鼠对可溶性血吸虫抗体制剂的即时（30分钟）皮肤试验和肥大细胞脱颗粒反应时，未观察到差异。上述发现表明，P品系小鼠在用辐照尾蚴免疫后产生IgM抗体反应的能力存在特异性缺陷。讨论了这种IgM反应缺陷对接种疫苗的P小鼠抵抗攻击感染能力下降的可能影响。
