ArticleThe Journal of experimental medicine2011
Critical role of the neutrophil-associated high-affinity receptor for IgE in the pathogenesis of experimental cerebral malaria.
Article in The Journal of experimental medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed.
- Myeloperoxidase and Other Markers of Neutrophil Activation Associate With Malaria and Malaria/HIV Coinfection in the Human Placenta.Frontiers in immunology · 2021Trial
- TLR9/NF-κB-mediated dendritic cell activation by neutrophil extracellular traps drives pathogenesis in experimental cerebral malaria.Journal of neuroinflammation · 2025Article
- Role of mast cell-derived exosomes in exacerbating neuronal injury of experimental cerebral malaria.Parasites & vectors · 2025Article
- The type 2 immune response in gut homeostasis and parasite transmission in malaria.Trends in parasitology · 2025Review
- Combining Transcriptomics and Proteomics to Screen Candidate Genes Related to Bovine Birth Weight.Animals : an open access journal from MDPI · 2024Article
- Pathogenetic mechanisms and treatment targets in cerebral malaria.Nature reviews. Neurology · 2023Review
- Basophil Depletion Alters Host Immunity, Intestinal Permeability, and Mammalian Host-to-Mosquito Transmission in Malaria.ImmunoHorizons · 2022Article
- Neutrophils in malaria: A double-edged sword role.Frontiers in immunology · 2022Review
- Article
- Trichinella spiralis co-infection exacerbates Plasmodium berghei malaria-induced hepatopathy.Parasites & vectors · 2020Article
- CXCR4 and MIF are required for neutrophil extracellular trap release triggered by Plasmodium-infected erythrocytes.PLoS pathogens · 2020Article
- Deficiency of immunoglobulin E protects mice from experimental abdominal aortic aneurysms.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Benign ethnic neutropenia.Blood reviews · 2019Review
- A case of mistaken identity: The MAR-1 antibody to mouse FcεRIα cross-reacts with FcγRI and FcγRIV.The Journal of allergy and clinical immunology · 2019Article
- Activation of Mast Cells PromoteFrontiers in cellular and infection microbiology · 2019Article
- Induction of Plasmodium-Specific Immune Responses Using Liposome-Based Vaccines.Frontiers in immunology · 2019Review
- Genetic analysis of cerebral malaria in the mouse model infected with Plasmodium berghei.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- TCRβ Combinatorial Immunoreceptor Expression by Neutrophils Correlates with Parasite Burden and Enhanced Phagocytosis during a Plasmodium berghei ANKA Malaria Infection.Infection and immunity · 2018Article
- Integrated pathogen load and dual transcriptome analysis of systemic host-pathogen interactions in severe malaria.Science translational medicine · 2018Article
- Transcriptomic Studies of Malaria: a Paradigm for Investigation of Systemic Host-Pathogen Interactions.Microbiology and molecular biology reviews : MMBR · 2018Review
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of the IgE-FcεRI complex in malaria severity in Plasmodium falciparum-hosting patients is unknown. We demonstrate that mice genetically deficient for the high-affinity receptor for IgE (FcεRIα-KO) or for IgE (IgE-KO) are less susceptible to experimental cerebral malaria (ECM) after infection with Plasmodium berghei (PbANKA). Mast cells and basophils, which are the classical IgE-expressing effector cells, are not involved in disease as mast cell-deficient and basophil-depleted mice developed a disease similar to wild-type mice. However, we show the emergence of an FcεRI(+) neutrophil population, which is not observed in mice hosting a non-ECM-inducing PbNK65 parasite strain. Depletion of this FcεRI(+) neutrophil population prevents ECM, whereas transfer of this population into FcεRIα-KO mice restores ECM susceptibility. FcεRI(+) neutrophils preferentially home to the brain and induce elevated levels of proinflammatory cytokines. These data define a new pathogenic mechanism of ECM and implicate an FcεRI-expressing neutrophil subpopulation in malaria disease severity.
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