Mountford A P, Coulson P S, Saunders N, Wilson R A
Department of Biology, University of York, UK.
J Immunol. 1989 Aug 1;143(3):989-95.
Partial resistance to reinfection developed in mice with immature infections of Schistosoma mansoni treated with the drug Ro11-3128, whereas mice vaccinated with irradiated cercariae and treated in a similar way did not become immune. Persistence of drug-treated parasites in the skin and draining lymph nodes, which prolonged the opportunity for efficient Ag presentation, was necessary for the development of protective immunity. Death and clearance of parasites solely in the skin, was not sufficient to induce protection. The expansion in the number of lymphocytes in the skin-draining nodes after vaccination, was reflected in the contrasting levels of resistance induced by the different drug-treatment regimes. Challenge parasites were eliminated predominantly after they reached the lungs. An investigation of antibody reactivity revealed an immunodominant response against a doublet of Ag of Mr 97 to 99 kDa. Recognition of this complex by antisera from different groups of mice was not related to their immune status. Western blots and inhibition analysis showed that this doublet has epitopes in common with the Sm97/paramyosin protective Ag, originally identified by antisera reactivity from mice immunized with a nonliving vaccine.
用药物Ro11 - 3128治疗的曼氏血吸虫未成熟感染小鼠产生了部分再感染抗性,而用辐照尾蚴免疫并以类似方式治疗的小鼠并未产生免疫。药物处理的寄生虫在皮肤和引流淋巴结中的持续存在延长了有效抗原呈递的机会,这是保护性免疫发展所必需的。仅寄生虫在皮肤中的死亡和清除不足以诱导保护作用。接种疫苗后皮肤引流淋巴结中淋巴细胞数量的增加反映在不同药物治疗方案所诱导的不同抗性水平上。攻击的寄生虫主要在到达肺部后被清除。抗体反应性研究揭示了针对分子量为97至99 kDa的双抗原的免疫显性反应。来自不同组小鼠的抗血清对该复合物的识别与它们的免疫状态无关。蛋白质免疫印迹和抑制分析表明,该双抗原与Sm97/副肌球蛋白保护性抗原具有共同表位,最初是通过用非活疫苗免疫的小鼠的抗血清反应性鉴定出来的。