Bickle Q D, Sacko M, Vignali D A
Department of Medical Parasitology, London School of Hygiene and Tropical Medicine.
Parasite Immunol. 1990 Nov;12(6):569-86. doi: 10.1111/j.1365-3024.1990.tb00989.x.
As with 20 krad-irradiated infections in mice, the present study shows that the immunity induced by Ro11-3128 termination of unattenuated infections at the skin stage is species specific, not operating against S. japonicum. Treatment with the drug Ro15-5458, also effective at the skin stage, however, resulted in significantly lower levels of resistance than Ro11-3128. Sera from mice immunized by infection plus Ro11-3128 treatment on days 1 or 2 (Ro11S) coprecipitated essentially the same pattern of 125I-labelled surface antigens as the 20 krad vaccine serum (VMS), viz. Mr 38,000, 32,000, 23,000 and 15,000. However, recognition by Ro11S was markedly stronger. Sera from the infected and Ro15-5458-treated mice (Ro15S) failed to recognize the Mr 23,000 antigen and produced a weaker response than Ro11S or VMS against the Mr 38,000 or 32,000 antigens but a comparable response to VMS against the Mr 15,000 antigen. Ro11S and VMS also recognized the Mr 16,000 surface antigen seen by Western blotting but its recognition by Ro15S was weaker. Compared with sera from animals treated at the skin stage, sera from animals treated at the lung stage (day + 6) showed weaker recognition of the Mr 32,000 and 15,000 antigens and no recognition of the Mr 23,000 antigen. In contrast, sera from mice treated at 15 days recognized both the Mr 32,000 and 23,000 antigens but not the Mr 15,000 antigen. Mice treated at these times show progressively less immunity than at the skin stage. Infected but untreated animals only showed significant recognition of the Mr 32,000 antigen. Thus compared with infections treated with Ro11-3128 on days 1 or 2, treatment at later times or with the drug Ro15-5458 resulted in selective and differential absence or diminution of response against either the Mr 38,000, 32,000, 23,000, 16,000 or 15,000 antigens. In vitro, Ro11-3128, in contrast to Ro15-5458, caused multiple vesicle formation at the surface of skin stage schistosomula but this was progressively less pronounced with lung and liver stage worms. The vesicles were shown to express surface membrane antigens but were apparently not derived from the existing outer leaflet of the surface membrane. It is suggested that this altered antigen expression might explain the optimum immunity induced.
与小鼠中20 krad辐照感染的情况一样，本研究表明，在皮肤期通过Ro11 - 3128终止未减毒感染所诱导的免疫具有物种特异性，对日本血吸虫不起作用。然而，在皮肤期也有效的药物Ro15 - 5458治疗所产生的抗性水平明显低于Ro11 - 3128。在第1天或第2天通过感染加Ro11 - 3128治疗免疫的小鼠血清（Ro11S）与20 krad疫苗血清（VMS）共沉淀出的125I标记表面抗原基本模式相同，即分子量为38,000、32,000、23,000和15,000。然而，Ro11S的识别明显更强。感染并经Ro15 - 5458治疗的小鼠血清（Ro15S）未能识别分子量为23,000的抗原，并且对分子量为38,000或32,000的抗原产生的反应比Ro11S或VMS弱，但对分子量为15,000的抗原产生的反应与VMS相当。Ro11S和VMS也识别通过蛋白质印迹法可见的分子量为16,000的表面抗原，但Ro15S对其的识别较弱。与在皮肤期治疗的动物血清相比，在肺期（第6天）治疗的动物血清对分子量为32,000和15,000的抗原的识别较弱，且未识别分子量为23,000的抗原。相比之下，在第15天治疗的小鼠血清识别分子量为32,000和23,000的抗原，但不识别分子量为15,000的抗原。在这些时间点治疗的小鼠显示出的免疫力比在皮肤期逐渐降低。感染但未治疗的动物仅对分子量为32,000的抗原表现出明显的识别。因此，与在第1天或第2天用Ro11 - 3128治疗的感染相比，在较晚时间治疗或用药物Ro15 - 5458治疗导致对分子量为38,000、32,000、23,000、16,000或15,000抗原的反应选择性地、差异性地缺失或减弱。在体外，与Ro15 - 5458相比，Ro11 - 3128在皮肤期血吸虫幼虫表面引起多个囊泡形成，但在肺期和肝期虫体中这种情况逐渐不明显。这些囊泡显示表达表面膜抗原，但显然不是源自表面膜现有的外小叶。有人认为这种改变的抗原表达可能解释了所诱导的最佳免疫。
