Albrecht Letusa, Angeletti Davide, Moll Kirsten, Blomqvist Karin, Valentini Davide, D'Alexandri Fabio Luiz, Maurer Markus, Wahlgren Mats
Department of Microbiology, Tumor- and Cell Biology (MTC), Karolinska Institutet, Stockholm, Sweden.
Therapeutic Immunology (TIM), Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden; CAST, Karolinska University Hospital, Huddinge, Sweden.
PLoS One. 2014 Dec 1;9(12):e113248. doi: 10.1371/journal.pone.0113248. eCollection 2014.
Plasmodium falciparum is the most lethal of the human malaria parasites. The virulence is associated with the capacity of the infected red blood cell (iRBC) to sequester inside the deep microvasculature where it may cause obstruction of the blood-flow when binding is excessive. Rosetting, the adherence of the iRBC to uninfected erythrocytes, has been found associated with severe malaria and found to be mediated by the NTS-DBL1α-domain of Plasmodium falciparum Erythrocyte Membrane Protein 1 (PfEMP1). Here we show that the reactivity of plasma of Cameroonian children with the surface of the FCR3S1.2-iRBC correlated with the capacity to disrupt rosettes and with the antibody reactivity with a recombinant PfEMP1 (NTS-DBL1α of IT4var60) expressed by parasite FCR3S1.2. The plasma-reactivity in a microarray, consisting of 96 overlapping 15-mer long peptides covering the NTS-DBL1α domain from IT4var60 sequence, was compared with their capacity to disrupt rosettes and we identified five peptides where the reactivity were correlated. Three of the peptides were localized in subdomain-1 and 2. The other two peptide-sequences were localized in the NTS-domain and in subdomain-3. Further, principal component analysis and orthogonal partial least square analysis generated a model that supported these findings. In conclusion, human antibody reactivity with short linear-peptides of NTS-DBL1α of PfEMP1 suggests subdomains 1 and 2 to hold anti-rosetting epitopes recognized by anti-rosetting antibodies. The data suggest rosetting to be mediated by the variable areas of PfEMP1 but also to involve structurally relatively conserved areas of the molecule that may induce biologically active antibodies.
恶性疟原虫是人类疟原虫中最致命的一种。其毒力与受感染红细胞(iRBC)在深部微血管内滞留的能力有关,当结合过度时,可能会导致血流阻塞。红细胞凝聚,即iRBC与未感染红细胞的黏附,已被发现与严重疟疾有关,并被认为是由恶性疟原虫红细胞膜蛋白1(PfEMP1)的NTS-DBL1α结构域介导的。在此,我们表明喀麦隆儿童血浆与FCR3S1.2-iRBC表面的反应性与破坏红细胞凝聚的能力以及与寄生虫FCR3S1.2表达的重组PfEMP1(IT4var60的NTS-DBL1α)的抗体反应性相关。在一个微阵列中,由覆盖IT4var60序列NTS-DBL1α结构域的96个重叠的15聚体长肽组成,将其血浆反应性与其破坏红细胞凝聚的能力进行比较,我们鉴定出五个反应性相关的肽段。其中三个肽段位于亚结构域1和2。另外两个肽段序列位于NTS结构域和亚结构域3。此外,主成分分析和正交偏最小二乘法分析生成了一个支持这些发现的模型。总之,人类与PfEMP1的NTS-DBL1α短线性肽的抗体反应性表明亚结构域1和2含有抗红细胞凝聚表位,可被抗红细胞凝聚抗体识别。数据表明红细胞凝聚由PfEMP1的可变区介导,但也涉及该分子结构上相对保守的区域,这些区域可能诱导产生生物活性抗体。