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首页> 外文会议>International Congress of Parasitology >Parasite-induced B-cell apoptosis results in loss of specific protective anti-trypanosome antibody responses, and abolishment of vaccine induced protective memory responses.
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Parasite-induced B-cell apoptosis results in loss of specific protective anti-trypanosome antibody responses, and abolishment of vaccine induced protective memory responses.

机译：寄生虫诱导的B细胞凋亡导致损失特异性保护性抗锥虫组抗体反应，以及废除疫苗诱导的保护性记忆反应。

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African trypanosomes are extracellular protozoan parasites that evade the host immune response by continuous antigenic variation of their surface coat. While this ensures the escape from antibody mediated clearance, in which IgMs play a major role, we have demonstrated that in addition, trypanosomes rapidly modulate the host B-cell compartment and disable the hosts' capacity to raise a specific IgM anti-parasite response. The analysis of different B cell populations showed that during early onset of a T. brucei infection, spleen remodeling results in the rapid and permanent loss of the IgM+ splenic marginal zone (MZ) B cell population. During infection these cells showed increased caspase activation and enzyme activity, indicating the initiation of apoptosis. When mimicking this event in vitro, by incubating trypanosome-specific IgM hybridoma cells with their corresponding parasite target, growth of the hybridoma cells was abrogated through cell-cell contact with trypanosomes. In vivo, infection-induced loss of IgM+MZ B cells coincided with the disappearance of protective variant-specific T-independent IgM responses, rendering mice rapidly susceptible to re-challenge with previously encountered variant antigenic type parasites. The latter suggests that during infection, no build-up of VSG-specific protective memory occurs. In addition, T. brucei infections abrogate vaccine induced protective responses to a non-related pathogen, underlining the severity of trypanosomiasis-induced B cell compartment destruction.
机译：非洲锥虫是胞外的原生动物寄生虫逃避通过表面涂层的连续抗原变异的宿主免疫应答。尽管这样可以确保从抗体介导的清除，其中的IgM起主要作用的逃逸，我们已经证明，此外，锥虫快速调节宿主的B细胞室和禁用主机的提高特定IgM抗寄生虫反应能力。表明，布氏锥虫感染的早期发作期间，脾重塑中的IgM +脾边缘区（MZ）的B细胞群的迅速和永久性丧失的结果不同B细胞群的分析。在感染过程中，这些细胞显示出增加的胱天蛋白酶活化和酶的活性，表明凋亡的启动。当模仿此事件在体外，通过温育锥虫特异性IgM杂交瘤细胞与其相应的寄生虫靶，杂交瘤细胞生长通过用锥虫细胞 - 细胞接触废止。在的IgM + MZ B细胞的体内，感染引起的损耗与保护特定变体无关的T-IgM的反应消失正值，渲染小鼠迅速易受再挑战与先前遇到的变体的抗原性类型的寄生虫。后者表明，感染期间，没有积聚VSG特异性保护存储器的发生。此外，布氏锥虫感染消除疫苗诱导到非相关病原体保护性应答，下划线锥虫病诱导的B细胞区室的破坏的严重性。

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