ArticleScientific reports2018
Detection of host pathways universally inhibited after Plasmodium yoelii infection for immune intervention.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 24 citations in OpenAlex.
- Temporal multi-tissue profiling reveals metabolites linked to immune response and malaria parasitemia control.iScience · 2026Article
- Immune Modulation by Plasmodium yoelii: Insights From Lethal and Non-Lethal Strains.Parasite immunology · 2026Review
- Emerging Role of Splenic Macrophage in Malaria Pathogenesis and Immunity.Immunity, inflammation and disease · 2025Review
- Dual nature of type I interferon responses and feedback regulations by SOCS1 dictate malaria mortality.Journal of advanced research · 2025Article
- Plasmodium yoelii as a model for malaria: insights into pathogenesis, drug resistance, and vaccine development.Molecular biology reports · 2025Review
- Malaria: Factors affecting disease severity, immune evasion mechanisms, and reversal of immune inhibition to enhance vaccine efficacy.PLoS pathogens · 2025Review
- Comparative genomics of Plasmodium yoelii nigeriensis N67 and N67C: genome-wide polymorphisms, differential gene expression, and drug resistance.BMC genomics · 2024Article
- Comparative analysis of peripheral whole blood transcriptome from asymptomatic carriers reveals upregulation of subsets of surface proteins implicated inBiochemistry and biophysics reports · 2024Article
- Dysfunction of CD169Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Article
- Malaria Genomics, Vaccine Development, and Microbiome.Pathogens (Basel, Switzerland) · 2023Review
- Genetic mapping of determinants in drug resistance, virulence, disease susceptibility, and interaction of host-rodent malaria parasites.Parasitology international · 2022Review
- Review
- Activation of cGAS-STING by Lethal Malaria N67C Dictates Immunity and Mortality through Induction of CD11bAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Pipecolic Acid, a Putative Mediator of the Encephalopathy of Cerebral Malaria and the Experimental Model of Cerebral Malaria.The Journal of infectious diseases · 2022Article
- The E3 ubiquitin ligase MARCH1 regulates antimalaria immunity through interferon signaling and T cell activation.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Accelerator or Brake: Immune Regulators in Malaria.Frontiers in cellular and infection microbiology · 2020Review
- Type I Interferons and Malaria: A Double-Edge Sword Against a Complex Parasitic Disease.Frontiers in cellular and infection microbiology · 2020Review
- Host-Malaria Parasite Interactions and Impacts on Mutual Evolution.Frontiers in cellular and infection microbiology · 2020Review
- Parasite-Related Genetic and Epigenetic Aspects and Host Factors InfluencingFrontiers in cellular and infection microbiology · 2018Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Malaria is a disease with diverse symptoms depending on host immune status and pathogenicity of Plasmodium parasites. The continuous parasite growth within a host suggests mechanisms of immune evasion by the parasite and/or immune inhibition in response to infection. To identify pathways commonly inhibited after malaria infection, we infected C57BL/6 mice with four Plasmodium yoelii strains causing different disease phenotypes and 24 progeny of a genetic cross. mRNAs from mouse spleens day 1 and/or day 4 post infection (p.i.) were hybridized to a mouse microarray to identify activated or inhibited pathways, upstream regulators, and host genes playing an important role in malaria infection. Strong interferon responses were observed after infection with the N67 strain, whereas initial inhibition and later activation of hematopoietic pathways were found after infection with 17XNL parasite, showing unique responses to individual parasite strains. Inhibitions of pathways such as Th1 activation, dendritic cell (DC) maturation, and NFAT immune regulation were observed in mice infected with all the parasite strains day 4 p.i., suggesting universally inhibited immune pathways. As a proof of principle, treatment of N67-infected mice with antibodies against T cell receptors OX40 or CD28 to activate the inhibited pathways enhanced host survival. Controlled activation of these pathways may provide important strategies for better disease management and for developing an effective vaccine.
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