Rasmussen K R, Kemp W M
Parasite Immunol. 1987 Mar;9(2):235-48. doi: 10.1111/j.1365-3024.1987.tb00503.x.
The interaction of the mouse complement system with adult male Schistosoma mansoni was studied by immunocytochemical localization procedures and in-vitro assays for complement mediated tegument damage. Mouse C3 was demonstrated to be associated with the parasite's tegument, but was localized only in the infoldings of the tegument and not on its free surface. Freshly harvested parasites manifested no detectable tegumental modification when incubated in normal mouse serum or in immune mouse serum. However, parasites which had been allowed to lose their adsorbed host components by elution (incubation in serum free media for 3 h at 37 degrees C) were severely damaged by incubation in normal mouse serum, but not by incubation in immune mouse serum. This damage was shown to be mediated by the alternative complement pathway and appeared to be initially limited to the tubercles of the adult male parasite. Tegument disruption could be blocked by pre-incubation of the eluted worms in either immune mouse serum or an IgG fraction of immune mouse serum. An IgG fraction of normal mouse serum did not protect the parasite, and infected mouse serum (IMS) which had been depleted of IgG produced tegument damage equivalent to that observed with normal mouse serum (NMS). The addition of I-IgG to NMS abrogated tegument damage. These data suggest that while adult schistosomes possess surface molecules bearing alternative pathway complement activation sites, these sites are masked by adsorbed host components in vivo. These results further indicate that in the absence of these masking host molecules anti-schistosome IgG may play a role in protecting the adult worm from alternative pathway activation, perhaps by binding to and blocking the activation sites on the tegument associated molecules.
通过免疫细胞化学定位程序和补体介导的皮层损伤体外试验，研究了小鼠补体系统与成年雄性曼氏血吸虫的相互作用。已证明小鼠C3与寄生虫的皮层相关，但仅定位于皮层的褶皱处，而非其游离表面。新鲜收获的寄生虫在正常小鼠血清或免疫小鼠血清中孵育时，未表现出可检测到的皮层修饰。然而，通过洗脱（在无血清培养基中于37℃孵育3小时）使其失去吸附的宿主成分的寄生虫，在正常小鼠血清中孵育时会受到严重损伤，但在免疫小鼠血清中孵育时则不会。这种损伤被证明是由替代补体途径介导的，并且最初似乎仅限于成年雄性寄生虫的结节。皮层破坏可通过将洗脱后的虫体预先在免疫小鼠血清或免疫小鼠血清的IgG组分中孵育来阻断。正常小鼠血清的IgG组分不能保护寄生虫，而去除了IgG的感染小鼠血清（IMS）产生的皮层损伤与正常小鼠血清（NMS）观察到的损伤相当。向NMS中添加I-IgG可消除皮层损伤。这些数据表明，虽然成年血吸虫具有带有替代途径补体激活位点的表面分子，但这些位点在体内被吸附的宿主成分所掩盖。这些结果进一步表明，在没有这些掩盖宿主分子的情况下，抗血吸虫IgG可能在保护成虫免受替代途径激活方面发挥作用，可能是通过结合并阻断皮层相关分子上的激活位点。
