Calderon J, Schreiber R D
Infect Immun. 1985 Nov;50(2):560-5. doi: 10.1128/iai.50.2.560-565.1985.
Entamoeba histolytica HM1 supported the activation of human alternative and classical complement pathways in the absence of ameba-reactive antibodies. Nonimmune serum depleted of C1q and factor D (NHS s C1q + D) and reconstituted with C1q was able to specifically deposit C3b onto trophozoites and produce lysis. This activity was not modified by the absorption of serum on E. histolytica. Serum depleted of factor B allowed C3b binding to amebae. Serum devoid of C4 effected only small amounts of C3 uptake. The kinetics of lysis of E. histolytica by serum in the presence of Mg-EGTA [ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid] (lacking classical pathway function) or by NHS s C1q + D and reconstituted with factor D was slow and only produced one-half the amount of lysis produced by NHS s C1q + D supplemented with C1q. These results indicate that the surface of the ameba can promote complement activation by the classical pathway, without the participation of specific antibodies, and that the magnitude of this activation is greater than that induced by the alternative pathway.
溶组织内阿米巴HM1在不存在抗阿米巴反应性抗体的情况下支持人替代补体途径和经典补体途径的激活。去除C1q和D因子的非免疫血清(NHS s C1q + D)并用C1q重构后能够特异性地将C3b沉积在滋养体上并产生溶解作用。这种活性不会因血清在溶组织内阿米巴上的吸附而改变。去除B因子的血清允许C3b与阿米巴结合。缺乏C4的血清仅导致少量的C3摄取。在存在Mg-EGTA [乙二醇双(β-氨基乙醚)-N,N,N',N'-四乙酸](缺乏经典途径功能)的情况下血清对溶组织内阿米巴的溶解动力学,或由NHS s C1q + D并用D因子重构后的血清对溶组织内阿米巴的溶解动力学缓慢,并且产生的溶菌量仅为补充C1q的NHS s C1q + D所产生溶菌量的一半。这些结果表明,阿米巴表面可在无特异性抗体参与的情况下通过经典途径促进补体激活,并且这种激活的程度大于替代途径所诱导的激活程度。