TRYPANOSOMA-BRUCEI VARIABLE SURFACE-ANTIGEN IS RELEASED BY DEGENERATING PARASITES BUT NOT BY ACTIVELY DIVIDING PARASITES
TRYPANOSOMA-BRUCEI VARIABLE SURFACE-ANTIGEN IS RELEASED BY DEGENERATING PARASITES BUT NOT BY ACTIVELY DIVIDING PARASITES
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DOI：
10.1111/j.1365-3024.1982.tb00435.x
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发表时间：
1982-01-01
影响因子：
2.2
通讯作者：
SENDASHONGA, CN
中科院分区：
文献类型：
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作者：
BLACK, SJ;HEWETT, RS;SENDASHONGA, CN
对单形型和多形型布氏毛滴虫表面抗原的生物合成和命运进行了研究，以评估细长和粗壮的布氏毛虫寄生虫如何将其变异的特异性糖蛋白(VSG)呈递给宿主免疫系统。单态和多态布氏毛滴虫在体外不释放新近合成的VSG。来自单态或多态种群的细长形布氏毛滴虫在体内不释放VSG。感染多形性寄生虫的受照小鼠血浆中游离VSG的检测与矮小的寄生虫的出现有关，可能是这些寄生虫退化的结果。体内释放的VSG与一些但不是所有针对VSG决定簇的抗体反应良好。与活体上的VSG反应的单抗和单特异性抗体不与释放的VSG反应，而不与活的布氏锥虫表面反应的VSG特异性单抗与释放的VSG反应。目前尚不清楚释放的VSG是否丢失了表达在锥体附着的VSG上的构象决定簇，也不清楚与活的锥虫上的VSG发生强烈反应的抗体是否亲和力太低而无法结合释放的VSG。显然，与释放的VSG相比，锥虫附着的VSG在刺激保护性体液反应方面更重要。其他地方报道了刺激保护性抗血管紧张素转换酶反应的要求(Sendashonga et Black，1982)。
Surface antigen biosynthesis and fate in monomorphic and pleomorphic T. brucei was examined to assess how slender and stumpy form T. brucei parasites present their variant specific glycoprotein (VSG) to the host immune system. Monomorphic and pleomorphic T. brucei did not release recently synthesized VSG in vitro. Slender form T. brucei, either from monomorphic or pleomorphic populations, did not release VSG in vivo. Detection of free VSG in plasma from irradiated mice infected with pleomorphic parasites correlated with the appearance of stumpy form parasites and possibly arose as a result of degeneration of those parasites. The in vivo release VSG was reacted well with some but not all antibodies directed against VSG determinants. Monoclonal and monospecific antibodies which react with VSG on living trypanosomes did not react with the released VSG, whereas VSG-specific monoclonal antibodies which do not react with the surface of living T. brucei did react with the released VSG. It was unclear whether released VSG had lost a conformational determinant expressed on trypanosome-attached VSG or whether antibodies which react strongly with VSG on living trypanosomes are of such low avidity that they fail to bind released VSG. Apparently, trypanosome-attached VSG is more important for stimulation of protective humoral responses than released VSG. The requirements for stimulation of protective anti-VSG responses are reported elsewhere (Sendashonga et Black, 1982).