Multiple Adhesive Phenotypes Linked to Rosetting Binding of Erythrocytes in
            <i>Plasmodium falciparum</i>
            Malaria

Fernández, Víctor; Treutiger, Carl Johan; Nash, GB; Wahlgren, Mats

doi:10.1128/iai.68.4.2391-2391.2000

Cited by 44 publications

(77 citation statements)

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“…The parasites were treated with trypsin/chymotrypsin for 1 h at 37°C with shaking before purification of schizonts to prevent the reinvasion of residual RBCs (29). The late-stage schizonts were purified by Percoll gradient centrifugation according to the protocol of Fernandez et al (30).…”

Section: Methodsmentioning

confidence: 99%

Human natural killer cells control Plasmodium falciparum infection by eliminating infected red blood cells

Chen

Amaladoss

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Immunodeficient mouse-human chimeras provide a powerful approach to study host-specific pathogens, such as Plasmodium falciparum that causes human malaria. Supplementation of immunodeficient mice with human RBCs supports infection by human Plasmodium parasites, but these mice lack the human immune system. By combining human RBC supplementation and humanized mice that are optimized for human immune cell reconstitution, we have developed RBC-supplemented, immune cell-optimized humanized (RICH) mice that support multiple cycles of P. falciparum infection. Depletion of human natural killer (NK) cells, but not macrophages, in RICH mice results in a significant increase in parasitemia. Further studies in vitro show that NK cells preferentially interact with infected RBCs (iRBCs), resulting in the activation of NK cells and the elimination of iRBCs in a contact-dependent manner. We show that the adhesion molecule lymphocyte-associated antigen 1 is required for NK cell interaction with and elimination of iRBCs. Development of RICH mice and validation of P. falciparum infection should facilitate the dissection of human immune responses to malaria parasite infection and the evaluation of therapeutics and vaccines. malaria infection | humanized mouse model | LFA-1 | NK killing

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Section: Methodsmentioning

confidence: 99%

Human natural killer cells control Plasmodium falciparum infection by eliminating infected red blood cells

Chen

Amaladoss

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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“…The P. falciparum laboratory clone FCR3S1.2 (17) and strains FCR3CSA (27), R29, Dd2, FCR3, PAvarO, and A4 (29) were cultivated as described previously (20). The phenotype of FCR3S1.2, PAvarO, and R29 iRBC was maintained by weekly enrichment over a Ficoll gradient (20), while FCR3CSA iRBC were frequently panned on chondroitin sulfate A (CSA) to maintain the parasite phenotype.…”

Section: Methodsmentioning

confidence: 99%

Generation of Cross-Protective Antibodies against Plasmodium falciparum Sequestration by Immunization with an Erythrocyte Membrane Protein 1-Duffy Binding-Like 1α Domain

et al. 2007

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The Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) is an important virulence factor on the surface of infected erythrocytes. Naturally acquired antibodies to PfEMP1 expressed by parasites causing severe malaria are suggested to be protective and of major interest for the development of a vaccine against severe disease. In this study, the PfEMP1 expressed by a parasite clone displaying a multiadhesive phenotype associated with severe malaria was well recognized by sera of malaria semi-immune children. The efficiency of the Duffy binding-like 1␣ (DBL1␣) domain of this PfEMP1 was therefore, alone or in combination with two additional DBL1␣ domains, evaluated as a potential vaccine candidate using both a rodent model and a primate model. Antibodies against the DBL1␣ domain were generated by immunization with recombinant DBL1␣-Semliki Forest virus particles and recombinant protein and analyzed in vitro. The immunized animals were challenged in vivo with various parasite strains or clones. Immunization with the PfEMP1-DBL1␣ domain abolished the PfEMP1-dependent sequestration of the homologous strain in immunized rats and substantially inhibited parasite adhesion in immunized monkeys. Protection against sequestration of heterologous parasite strains was also confirmed by direct or indirect challenge in the rat model. These results strongly support the use of the DBL1␣ domain in the development of a vaccine targeting severe malaria.

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“…Enriched trophozoite and schizont preparations used in Western blot analysis were obtained by Percoll purification (29). Ring stage parasites (ϳ5% parasitemia) were transfected with 80 g of purified plasmid DNA (Plasmid Maxi Kit; Qiagen) as previously described (30) except using modified electroporation conditions (31).…”

Section: Methodsmentioning

confidence: 99%

A Subset of Plasmodium falciparum SERA Genes Are Expressed and Appear to Play an Important Role in the Erythrocytic Cycle

Miller¹,

Good

Drew³

et al. 2002

Journal of Biological Chemistry

160

173

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The Plasmodium falciparum serine repeat antigen (SERA) has shown considerable promise as a blood stage vaccine for the control of malaria. A related protein, SERPH, has also been described in P. falciparum. Whereas their biological role remains unknown, both proteins possess papain-like protease domains that may provide attractive targets for therapeutic intervention. Genomic sequencing has recently shown that SERA and SERPH are the fifth and sixth genes, respectively, in a cluster of eight SERA homologues present on chromosome 2. In this paper, the expression and functional relevance of these eight genes and of a ninth SERA homologue found on chromosome 9 were examined in blood stage parasites. Using reverse transcriptase-PCR and microarray approaches, we demonstrate that whereas mRNA to all nine SERA genes is synthesized late in the erythrocytic cycle, it is those genes in the central region of the chromosome 2 cluster that are substantially up-regulated at this time. Using antibodies specific to each SERA, it was apparent that SERA4 to -6, and possibly also SERA9, are synthesized in blood stage parasites. The reactivity of antibodies from malaria-immune individuals with the SERA recombinant proteins suggested that SERA2 and SERA3 are also expressed at least in some parasite populations. To examine whether SERA genes are essential to blood stage growth, each of the eight chromosome 2 SERA genes was targeted for disruption. Whereas genes at the periphery of the cluster were mostly dispensable (SERA2 and -3 and SERA7 and -8), those in the central region (SERA4 to -6) could not be disrupted. The inability to disrupt SERA4, -5, and -6 is consistent with their apparent dominant expression and implies an important role for these genes in maintenance of the erythrocytic cycle.

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Multiple Adhesive Phenotypes Linked to Rosetting Binding of Erythrocytes in Plasmodium falciparum Malaria

Cited by 44 publications

References 0 publications

Human natural killer cells control Plasmodium falciparum infection by eliminating infected red blood cells

Human natural killer cells control Plasmodium falciparum infection by eliminating infected red blood cells

Generation of Cross-Protective Antibodies against Plasmodium falciparum Sequestration by Immunization with an Erythrocyte Membrane Protein 1-Duffy Binding-Like 1α Domain

A Subset of Plasmodium falciparum SERA Genes Are Expressed and Appear to Play an Important Role in the Erythrocytic Cycle

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