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首页> 外文期刊>Infection and immunity >Antibody-mediated shift in the profile of glycoprotein A phenotypes observed in a mouse model of Pneumocystis carinii pneumonia.
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Antibody-mediated shift in the profile of glycoprotein A phenotypes observed in a mouse model of Pneumocystis carinii pneumonia.

机译：在卡氏肺孢子虫肺炎的小鼠模型中观察到的糖蛋白A表型的抗体介导的转变。

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摘要

It is well established that Pneumocystis carinii has the molecular capability for variation of a major surface antigen, glycoprotein A (gpA). However, the extent of expression of gpA variation among P. carinii organisms infecting a single host and whether this variation has any impact on host-parasite immunological interactions is unknown. Using a mouse model of P. carinii pneumonia, we were able to demonstrate the expression of more than one gpA phenotype in a closed population of infected mice. Administration of monoclonal antibody (MAb) 2B5, which is specific for one of the gpA phenotypes, resulted in a marked diminution in the frequency of this particular gpA phenotype in the population of organisms. This effect was due to a loss of trophozoites bearing the specific epitope recognized by MAb 2B5; cysts bearing the same epitope appeared unaffected. Interestingly, P. carinii was unable to introduce a new phenotype into the population to compensate for the loss of trophozoites bearing the epitope recognized by MAb 2B5. Discontinuing administration of MAb 2B5 allowed the MAb 2B5-binding phenotype to reemerge. This finding suggests that the phenotype recognized by MAb 2B5 was continually produced even when MAb 2B5 was present. Thus, although P. carinii exhibited a form of antigenic variation, it did not appear able to rapidly introduce new phenotypes into the population in response to destruction by antibodies.
机译：众所周知，卡氏肺孢子虫具有改变主要表面抗原糖蛋白A（gpA）的分子能力。但是，尚不知道感染单个宿主的卡氏疟原虫生物中gpA变异的表达程度以及该变异是否对寄主-寄生虫的免疫相互作用有影响。使用卡氏疟原虫肺炎的小鼠模型，我们能够证明在封闭的受感染小鼠群体中一种以上gpA表型的表达。对一种gpA表型具有特异性的单克隆抗体（MAb）2B5的使用导致该特定gpA表型在生物种群中的出现频率显着降低。该作用归因于带有MAb 2B5识别的特定表位的滋养体的损失;带有相同表位的囊肿似乎未受影响。有趣的是，卡氏疟原虫不能将新的表型引入种群中，以补偿带有MAb 2B5识别的表位的滋养体的损失。停止施用MAb 2B5使MAb 2B5结合表型重新出现。该发现表明即使存在MAb 2B5，MAb 2B5识别的表型仍持续产生。因此，尽管卡氏疟原虫表现出某种形式的抗原变异，但它似乎不能响应于抗体的破坏而迅速将新的表型引入种群。

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