Characterization of domains of the phosphoriboprotein P0 of Plasmodium falciparum

Chatterjee, Sourish; Singh, Subhash; Sohoni, Rashmi; Kattige, Vidya G.; Deshpande, Charusheela; Chiplunkar, Shubhada V.; Kumar, Nirbhay; Sharma, Shobhona

doi:10.1016/s0166-6851(99)00226-1

Cited by 32 publications

(41 citation statements)

References 30 publications

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“…Three peptides corresponding to N-and C-terminal regions of PfP0 were synthesized and purified to 70 to 80% (Chiron Corp., Clayton, Victoria, Australia). The peptides were designated N1 (DNVGSNQMASVRKSLR; codons 33 to 48), N2 (SVRKSLRGKATILMGKNT; codons 42 to 59), and C1 (AKADEPKKEEAKKVE; codons 285 to 299), and correspond to T-cell epitopes identified by lymphocyte proliferation responses of immunized mice (6). A purified GMP grade recombinant protein corresponding to region II of EBA-175 (codons 144 to 753) was expressed in baculovirus (36) and kindly provided by David Narum, Malaria Vaccine Development Unit, National Institutes of Health, Bethesda, Md.…”

Section: Materials and Methods Study Populationmentioning

confidence: 99%

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Distinct Th1- and Th2-Type Prenatal Cytokine Responses toPlasmodium falciparumErythrocyte Invasion Ligands

Malhotra

Mungai

Muchiri³

et al. 2005

Infect Immun

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106

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Section: Materials and Methods Study Populationmentioning

confidence: 99%

“…PfP0 is the least studied of the three antigens. The protein is expressed on the merozoite surface and polyclonal antibodies to its N-and C-terminal domains inhibit P. falciparum growth in vitro (6,7). Naturally acquired antibodies to PfP0 in adults residing in areas of India and Africa in which malaria is endemic are detectable (37).…”

Section: Vol 73 2005mentioning

confidence: 99%

Distinct Th1- and Th2-Type Prenatal Cytokine Responses toPlasmodium falciparumErythrocyte Invasion Ligands

Malhotra

Mungai

Muchiri³

et al. 2005

Infect Immun

Self Cite

106

View full text Add to dashboard Cite

show abstract

“…Three peptides corresponding to N-and C-terminal regions of PfP0 were synthesized and purified to 70-80% (Chiron, Clayton, Victoria, Australia). The peptides were designated N1 (DNVGSNQMASVRKSLR; codons 33-48), N2 (SV-RKSLRGKATILMGKNT; codons [42][43][44][45][46][47][48][49][50][51][52][53][54][55][56][57][58][59], and C1 (AKADEPKKEE-AKKVE; codons 285-299) and correspond to T cell epitopes identified by lymphocyte proliferation responses of immunized mice (41). PHA (Sigma-Aldrich) or anti-CD3/28-coated T cell expander beads (Dynal) were used as positive controls.…”

Section: Ags and Mitogensmentioning

confidence: 99%

Human Cord Blood CD4+CD25hi Regulatory T Cells Suppress Prenatally Acquired T Cell Responses toPlasmodium falciparumAntigens

Mackroth

Malhotra

Mungai

et al. 2011

The Journal of Immunology

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In malaria endemic regions, a fetus is often exposed in utero to Plasmodium falciparum blood-stage Ags. In some newborns, this can result in the induction of immune suppression. We have previously shown these modulated immune responses to persist postnatally, with a subsequent increase in a child’s susceptibility to infection. To test the hypothesis that this immune suppression is partially mediated by malaria-specific regulatory T cells (Tregs) in utero, cord blood mononuclear cells (CBMC) were obtained from 44 Kenyan newborns of women with and without malaria at delivery. CD4+CD25lo T cells and CD4+CD25hi FOXP3+ cells (Tregs) were enriched from CBMC. Treg frequency and HLA-DR expression on Tregs were significantly greater for Kenyan as compared with North American CBMC (p < 0.01). CBMC/CD4+ T cells cultured with P. falciparum blood-stage Ags induced production of IFN-γ, IL-13, IL-10, and/or IL-5 in 50% of samples. Partial depletion of CD25hi cells augmented the Ag-driven IFN-γ production in 69% of subjects with malaria-specific responses and revealed additional Ag-reactive lymphocytes in previously unresponsive individuals (n = 3). Addition of Tregs to CD4+CD25lo cells suppressed spontaneous and malaria Ag-driven production of IFN-γ in a dose-dependent fashion, until production was completely inhibited in most subjects. In contrast, Tregs only partially suppressed malaria-induced Th2 cytokines. IL-10 or TGF-β did not mediate this suppression. Thus, prenatal exposure to malaria blood-stage Ags induces Tregs that primarily suppress Th1-type recall responses to P. falciparum blood-stage Ags. Persistence of these Tregs postnatally could modify a child’s susceptibility to malaria infection and disease.

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“…This protein was described as an immunodominant antigen recognized by sera from both patients and animals infected with Leishmania chagasi-L. infantum (30,33). In addition, antibodies against the Plasmodium falciparum P0 phosphoprotein were detected extensively in malaria-immune persons, but not in malaria patients (5). Interestingly, antibodies against ribosomal P0 were found to protect mice against experimental infection with Plasmodium yoelii (6).…”

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TheLeishmania infantumAcidic Ribosomal Protein P0 Administered as a DNA Vaccine Confers Protective Immunity toLeishmania majorInfection in BALB/c Mice

et al. 2003

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In this study, we examined the immunogenic properties of the Leishmania infantum acidic ribosomal protein P0 (LiP0) in the BALB/c mouse model. The humoral and cellular responses induced by the administration of the LiP0 antigen, either as soluble recombinant LiP0 (rLiP0) or as a plasmid DNA formulation (pcDNA3-LiP0), were determined. Also, the immunological response associated with a prime-boost strategy, consisting of immunization with pcDNA3-LiP0 followed by a boost with rLiP0, was assayed. Immunization with rLiP0 induced a predominant Th2-like humoral response, but no anti-LiP0 antibodies were induced after immunization with pcDNA3-LiP0, whereas a strong humoral response consisting of a mixed immunoglobulin G2a (IgG2a)-IgG1 isotype profile was induced in mice immunized with the prime-boost regime. For all three immunization protocols, rLiP0-stimulated production of gamma interferon (IFN-␥) in both splenocytes and lymph node cells from immunized mice was observed. However, it was only when mice were immunized with pcDNA3-LiP0 that noticeable protection against L. major infection was achieved, as determined by both lesion development and parasite burden. Immunization of mice with LiP0-DNA primes both CD4؉ and CD8 ؉ T cells, which, with the L. major challenge, were boosted to produce significant levels of IL-12-dependent, antigen-specific IFN-␥. Taken together, these data indicate that genetic vaccination with LiP0 induces protective immunological effector mechanisms, yet the immunological response elicited by LiP0 is not sufficient to keep the infection from progressing.

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Characterization of domains of the phosphoriboprotein P0 of Plasmodium falciparum

Cited by 32 publications

References 30 publications

Distinct Th1- and Th2-Type Prenatal Cytokine Responses toPlasmodium falciparumErythrocyte Invasion Ligands

Distinct Th1- and Th2-Type Prenatal Cytokine Responses toPlasmodium falciparumErythrocyte Invasion Ligands

Human Cord Blood CD4+CD25hi Regulatory T Cells Suppress Prenatally Acquired T Cell Responses toPlasmodium falciparumAntigens

TheLeishmania infantumAcidic Ribosomal Protein P0 Administered as a DNA Vaccine Confers Protective Immunity toLeishmania majorInfection in BALB/c Mice

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