Dwyer D M
J Immunol. 1976 Dec;117(6):2081-91.
The effects of specific antibodies on the surface membrane antigens of Leishmania donovani (strain 1S, clone 2D) amastigote and promastigote developmental stages was detected in vitro by using several direct and indirect immunofluorescence methods. Stage specific anti-L. donovani sera and sera from L. donovani-infected hamsters induced parasite surface membrane antigens to aggregate, move along the longitudinal cell axis, form polar cell caps, and subsequently disappear. No membrane fluorescence was observed in cells treated identically with normal sera. In amastigotes in a single anterior cell pole cap was formed after antibody treatment. However, antibody-treated promastigotes showed tripartite membrane antigen capping consisting of a major anterior cell pole cap with minor caps at the posterior cell pole and flagellar tip regions. Loss of surface fluorescence from the two latter capped cell regions was frequently concurrent with the formation of extracellular fluorescent plasmanemes. The cell-capping process was antibody concentration, temperature, time, and energy dependent. No cell caps were formed at low temperature or in the presence of several metabolic inhibitors. Cell cap formation was also selectively inhibited by certain types of antibody-induced intercellular agglutination. Parasite membrane antigens removed by capping were regenerated and detectable at the cell surface only after a 3.5 to 4-hr period. Antibody-induced membrane antigen movement in L. donovani is apparently similar to pheonmena observed with mammalian cells. Results of direct cross-staining and cross-absorption cell-capping experiments showed that the two parasite developmental forms shared some common or at least cross-reacting membrane antigens and that each form also possessed some unique stage-specific surface antigens. Cell-capping results with sera from L. donovani infected hamsters showed that this host produces some IgG which is directed specifically against certain parasite surface membrane antigens. The results suggest that host antibody-induced parasite membrane antigen modulation might have a role in the infectious process of this human pathogen.
采用多种直接和间接免疫荧光法，在体外检测了特异性抗体对杜氏利什曼原虫（1S株，2D克隆）无鞭毛体和前鞭毛体发育阶段表面膜抗原的影响。阶段特异性抗杜氏利什曼原虫血清以及来自感染杜氏利什曼原虫仓鼠的血清可诱导寄生虫表面膜抗原聚集，沿细胞纵轴移动，形成极性细胞帽，随后消失。用正常血清进行相同处理的细胞未观察到膜荧光。抗体处理后，无鞭毛体在单个前细胞极形成帽。然而，抗体处理的前鞭毛体显示出三方膜抗原帽，由主要的前细胞极帽和后细胞极及鞭毛尖端区域的小帽组成。后两个被帽覆盖的细胞区域表面荧光的丧失常常与细胞外荧光质膜的形成同时发生。细胞帽形成过程依赖于抗体浓度、温度、时间和能量。在低温或存在几种代谢抑制剂的情况下不形成细胞帽。细胞帽的形成也会被某些类型的抗体诱导的细胞间凝集选择性抑制。通过帽形成去除的寄生虫膜抗原仅在3.5至4小时后在细胞表面重新生成并可检测到。抗体诱导的杜氏利什曼原虫膜抗原移动显然类似于在哺乳动物细胞中观察到的现象。直接交叉染色和交叉吸收细胞帽实验结果表明，两种寄生虫发育形式共享一些共同的或至少交叉反应的膜抗原，并且每种形式也具有一些独特的阶段特异性表面抗原。用感染杜氏利什曼原虫仓鼠的血清进行细胞帽实验结果表明，这种宿主产生一些特异性针对某些寄生虫表面膜抗原的IgG。结果表明，宿主抗体诱导的寄生虫膜抗原调节可能在这种人类病原体的感染过程中起作用。
