摘要

BACKGROUND: Bilharzia is one of the major parasitic infections affecting the public health and socioeconomic circumstances in (sub) tropical areas. Its causative agents are schistosomes. Since these worms remain in their host for decades, they have developed mechanisms to evade or resist the immune system. Like several other parasites, their surface membranes are coated with a protective layer of glycoproteins that are anchored by a lipid modification. METHODS AND FINDINGS: We studied the release of glycosyl-phosphatidylinositol (GPI)-anchored proteins of S. mansoni and found them in the circulation associated with host lipoprotein particles. Host cells endocytosed schistosomal GPI-anchored proteins via their lipoprotein receptor pathway, resulting in disturbed lysosome morphology. In patients suffering from chronic schistosomiasis, antibodies attacked the parasite GPI-anchored glycoproteins that were associated with the patients' own lipoprotein particles. These immunocomplexes were endocytosed by cells carrying an immunoglobulin-Fc receptor, leading to clearance of lipoproteins by the immune system. As a consequence, neutral lipids accumulated in neutrophils of infected hamsters and in human neutrophils incubated with patient serum, and this accumulation was associated with apoptosis and reduced neutrophil viability. Also, Trypanosoma brucei, the parasite that causes sleeping sickness, released its major GPI-anchored glycoprotein VSG221 on lipoprotein particles, demonstrating that this process is generalizable to other pathogens/parasites. CONCLUSIONS: Transfer of parasite antigens to host cells via host lipoproteins disrupts lipid homeostasis in immune cells, promotes neutrophil apoptosis, may result in aberrant antigen presentation in host cells, and thus cause an inefficient immune response against the pathogen.

译文

背景: 在 (次) 热带地区,天蛾是影响公共健康和社会经济环境的主要寄生虫感染之一。它的病原体是血吸虫。由于这些蠕虫在它们的宿主中存在了几十年,它们已经形成了逃避或抵抗免疫系统的机制。像其他几种寄生虫一样,它们的表面膜覆盖着一层糖蛋白保护层,由脂质修饰固定。方法和结果: 我们研究了曼氏体的糖基磷脂酰肌醇 (GPI) 锚定蛋白的释放,并发现它们存在于与宿主脂蛋白颗粒相关的循环中。宿主细胞通过其脂蛋白受体途径内吞血吸虫 GPI 锚定蛋白,导致溶酶体形态紊乱。在患有慢性血吸虫病的患者中,抗体攻击与患者自身脂蛋白颗粒相关的寄生虫 GPI 锚定糖蛋白。这些免疫复合物被携带免疫球蛋白 Fc 受体的细胞内吞,导致免疫系统清除脂蛋白。因此,中性脂质在受感染仓鼠的中性粒细胞和与患者血清一起孵育的人中性粒细胞中积累,这种积累与细胞凋亡和中性粒细胞活性降低有关。此外,引起昏睡病的寄生虫布氏锥虫在脂蛋白颗粒上释放了其主要的 GPI 锚定糖蛋白 VSG221,表明这一过程可推广到其他病原体/寄生虫。结论: 通过宿主脂蛋白将寄生虫抗原转移到宿主细胞会破坏免疫细胞中的脂质稳态,促进中性粒细胞凋亡,可能导致宿主细胞中的异常抗原呈递, 从而导致对病原体的低效免疫反应。

endocytosis

肿瘤 机制与治疗 临床研究术语
概述  :  

在细胞的新陈代谢过程中,不断有各种物质进出细胞,这些物质包括一些离子、小分子物质、大分子物质及一些颗粒物质。大分子物质及颗粒性物质不能穿过细胞膜,是以另外一种特殊方式来进行跨细胞膜转运的,以及物质在进出细胞的转运过程中都是由膜包裹、形成囊泡、与膜融合或断裂使细胞外物质进入细胞内。这就是目前公认的生物体摄取生物大分子的主要途径-内吞作用。内吞作用,又叫入胞作用或胞吞作用,是指真核生物细胞通过在质膜位置处形成囊泡从细胞外部环境吸收营养物质的过程,细胞的内吞作用使得细胞外的大分子物质得以内化从而进

Endocytosis   英 /,endəʊsaɪ'təʊsɪs/   美 /,ɛndosaɪ'tosɪs/

释    义   n. [细胞] 内吞作用;复数 endocytoses

例    句   The established view in cellular biology dictates that the cellular internalization of hydrophilic macromolecules can only be achieved through the classical endocytosis pathway. 传统细胞生物学的观点认为:亲水性大分子只能通过经典的胞吞作用才能实现细胞内在化。

请扫描右侧二维码,免费查看词汇专业知识背景