...
首页> 外文期刊>Transfusion medicine >In vitro RBC exposure to Plasmodium falciparum has no effect on RBC antigen expression.
【24h】

In vitro RBC exposure to Plasmodium falciparum has no effect on RBC antigen expression.

机译:体外RBC暴露于恶性疟原虫对RBC抗原表达没有影响。

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

       

摘要

Severe malarial anaemia is a leading cause of death in African children younger than 3 years of age who are infected with Plasmodium falciparum. The pathogenesis of this anaemia is not understood. The purpose of this study was to determine if P. falciparum induces changes in RBC membranes that contribute to the immune destruction of RBCs. RBCs were collected from healthy subjects and tested using standard haemagglutination assays for 45 antigens representing 21 blood group systems/collections before and after exposure to P. falciparum, strain FVO. Lectins were used to determine whether crypt or neoantigens were expressed on the RBC membrane. Polybrene was used to detect changes in sialic acid. RBCs were cultured in vitro with and without the parasite, and blinded serologic studies were completed. CD35 (complement receptor 1), CD55 (decay-accelerating factor), CD59 (membrane inhibitor of reactive lysis) and CD47 (integrin-associated protein) flow cytometric assays were compared for infected and uninfected RBCs. The percentage of parasitaemia was determined using Giemsa-stained thin blood films. Two (Ch, Lub) of the 45 antigens had differing strengths of agglutination between infected and uninfected RBCs, but these differences were resolved with a second source of antisera. Forty-three antigens showed no significant differences in the strength of agglutination between the infected and uninfected RBCs. Lectin and polybrene testing showed no differences. CD35, CD55, CD59 and CD47 levels showed no significant differences. P. falciparum does not appear to alter the expression of classified immunogenic antigens on the RBC membrane in this in vitro system. The pathogenesis of the haemolytic episode that occurs in these children remains unclear.
机译:严重的疟疾贫血是感染恶性疟原虫的3岁以下非洲儿童的主要死亡原因。这种贫血的发病机理尚不清楚。这项研究的目的是确定恶性疟原虫是否诱导RBC膜发生变化,从而有助于RBC的免疫破坏。从健康受试者收集红细胞,并使用标准血凝测定法对代表恶性疟原虫菌株FVO之前和之后的21种血型系统/集合的45种抗原进行测试。用凝集素确定在RBC膜上是否表达了隐窝或新抗原。聚乙烯用于检测唾液酸的变化。在有或没有寄生虫的情况下体外培养红细胞,并完成了盲法血清学研究。比较了CD35(补体受体1),CD55(衰变促进因子),CD59(反应性裂解的膜抑制剂)和CD47(整合素相关蛋白)流式细胞术检测感染和未感染的RBC的情况。使用吉姆萨染色的薄血膜测定寄生虫血症的百分比。 45种抗原中的两种(Ch,Lub)在受感染和未受感染的RBC之间具有不同的凝集强度,但这些差异可以通过第二种抗血清来源解决。 43种抗原在感染和未感染的RBC之间的凝集强度没有显着差异。凝集素和聚乙烯的测试没有差异。 CD35,CD55,CD59和CD47水平没有显着差异。在该体外系统中,恶性疟原虫似乎并未改变分类的免疫原性抗原在RBC膜上的表达。在这些儿童中发生的溶血发作的发病机理仍不清楚。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号