ArticleInfection and immunity2007
Macrophage-mediated but gamma interferon-independent innate immune responses control the primary wave of Plasmodium yoelii parasitemia.
Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 90 citations in OpenAlex.
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- Immune Modulation by Plasmodium yoelii: Insights From Lethal and Non-Lethal Strains.Parasite immunology · 2026Review
- Plasmodium yoelii as a model for malaria: insights into pathogenesis, drug resistance, and vaccine development.Molecular biology reports · 2025Review
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- Aspecific binding of anti-NK1.1 antibodies on myeloid cells in an experimental model for malaria-associated acute respiratory distress syndrome.Malaria journal · 2024Article
- NK cells contribute to the resolution of experimental malaria-associated acute respiratory distress syndrome after antimalarial treatment.Frontiers in immunology · 2024Article
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- Comparative transcriptomic analysis reveals translationally relevant processes in mouse models of malaria.eLife · 2022Article
- Macrophage migration inhibitory factor contributes to immunopathogenesis duringFrontiers in cellular and infection microbiology · 2022Article
- The plasma membrane calcium ATPase 4 does not influence parasite levels but partially promotes experimental cerebral malaria during murine blood stage malaria.Malaria journal · 2021Article
- B cell intrinsic expression of IFNλ receptor suppresses the acute humoral immune response to experimental blood-stage malaria.Virulence · 2020Article
- Contributions of IFN-γ and granulysin to the clearance of Plasmodium yoelii blood stage.PLoS pathogens · 2020Article
- Using two phases of the CD4 T cell response to blood-stage murine malaria to understand regulation of systemic immunity and placental pathology in Plasmodium falciparum infection.Immunological reviews · 2020Review
- Article
- Co-infection: the outcome of Plasmodium infection differs according to the time of pre-existing helminth infection.Parasitology research · 2018Article
- A Plasmodium yoelii HECT-like E3 ubiquitin ligase regulates parasite growth and virulence.Nature communications · 2017Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
In most models of blood-stage malaria infection, proinflammatory immune responses are required for control of infection and elimination of parasites. We hypothesized therefore that the fulminant infections caused in mice by the lethal strain of Plasmodium yoelii (17XL) might be due to failure to activate a sufficient inflammatory response. Here we have compared the adaptive CD4+ T-cell and innate immune response to P. yoelii 17XL with that induced by the self-resolving, nonlethal strain of P. yoelii, 17X(NL). During the first 7 to 9 days of infection, splenic effector CD4+ T-cell responses were similar in mice with lethal and nonlethal infections with similar levels of activation in vivo and equivalent proliferation in vitro following mitogenic stimulation. Nonspecific T-cell hyporesponsiveness was observed at similar levels during both infections and was due, in part, to suppression mediated by CD11b+ cells. Importantly, however, RAG-/- mice were able to control the initial growth phase of nonlethal P. yoelii infection as effectively as wild-type mice, indicating that T cells and/or B cells play little, if any, role in control of the primary peak of parasitemia. Somewhat unexpectedly, we could find no clear role for either NK cells or gamma interferon (IFN-gamma) in controlling primary P. yoelii infection. In contrast, depletion of monocytes/macrophages exacerbated parasite growth and anemia during both lethal and nonlethal acute P. yoelii infections, indicating that there is an IFN-gamma-, NK cell-, and T-cell-independent pathway for induction of effector macrophages during acute malaria infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.