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首页> 外文期刊>Infection and immunity >Trypanosomes Expressing a Mosaic Variant Surface Glycoprotein Coat Escape Early Detection by the Immune System
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Trypanosomes Expressing a Mosaic Variant Surface Glycoprotein Coat Escape Early Detection by the Immune System

机译：锥虫表达马赛克变异表面糖蛋白外套逃脱免疫系统的早期检测。

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Host resistance to African trypanosomiasis is partially dependent on an early and strong T-independent B-cell response against the variant surface glycoprotein (VSG) coat expressed by trypanosomes. The repetitive array of surface epitopes displayed by a monotypic surface coat, in which identical VSG molecules are closely packed together in a uniform architectural display, cross-links cognate B-cell receptors and initiates T-independent B-cell activation events. However, this repetitive array of identical VSG epitopes is altered during the process of antigenic variation, when former and nascent VSG proteins are transiently expressed together in a mosaic surface coat. Thus, T-independent B-cell recognition of the trypanosome surface coat may be disrupted by the introduction of heterologous VSG molecules into the coat structure. To address this hypothesis, we transformed Trypanosoma brucei rhodesiense LouTat 1 with the 117 VSG gene from Trypanosoma brucei brucei MiTat 1.4 in order to produce VSG double expressers; coexpression of the exogenous 117 gene along with the endogenous LouTat 1 VSG gene resulted in the display of a mosaic VSG coat. Results presented here demonstrate that the host's ability to produce VSG-specific antibodies and activate B cells during early infection with VSG double expressers is compromised relative to that during infection with the parental strain, which displays a monotypic coat. These findings suggest a previously unrecognized mechanism of immune response evasion in which coat-switching trypanosomes fail to directly activate B cells until coat VSG homogeneity is achieved. This process affords an immunological advantage to trypanosomes during the process of antigenic variation.
机译：宿主对非洲锥虫病的抗药性部分取决于对锥虫体表达的变异表面糖蛋白（VSG）皮层的早期且强烈的T非依赖性B细胞应答。由单型表面涂层显示的表面抗原决定簇的重复阵列，其中相同的VSG分子在统一的体系结构展示中紧密堆积在一起，交联同源的B细胞受体并引发不依赖T的B细胞活化事件。但是，当以前的和新生的VSG蛋白在镶嵌表面涂层中一起瞬时表达时，相同的VSG表位的这种重复排列会在抗原变异过程中发生改变。因此，可通过将异源VSG分子引入衣壳结构来破坏锥虫表面衣壳的T依赖性B细胞识别。为了解决这个假设，我们用MiTat 1.4中的TryTryosos brucei brucei MiTat 1.4的117个VSG基因转化了LouTat 1小鼠，以产生VSG双表达。外源117基因与内源LouTat 1 VSG基因的共表达导致显示镶嵌VSG外壳。此处显示的结果表明，与VSG双表达的早期感染相比，宿主产生VSG特异性抗体和激活B细胞的能力相对于亲本菌株（表现出单型外壳）感染的能力受到损害。这些发现提示了先前无法识别的逃避免疫反应的机制，其中换衣的锥虫无法直接激活B细胞，直到达到外套VSG的同质性。该过程在抗原变异过程中为锥虫提供了免疫学上的优势。

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