ArticleInfection and immunity2013
IgG and IgE collaboratively accelerate expulsion of Strongyloides venezuelensis in a primary infection.
Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Circulating Leukocytes and Antibody Isotype Reactivity in Rats Experimentally Infected with Different Burdens ofTropical medicine and infectious disease · 2026Article
- Maternal IgE Influence on Fetal and Infant Health.Immunological reviews · 2025Review
- The role of immunoglobulin E in non-atopic disorders.Frontiers in immunology · 2025Review
- Review
- Class switching is differentially regulated in RBC alloimmunization and vaccination.Transfusion · 2023Article
- Sialylation as an Important Regulator of Antibody Function.Frontiers in immunology · 2022Review
- Context-dependent roles of B cells during intestinal helminth infection.PLoS neglected tropical diseases · 2021Review
- Mast Cell Modulation of B Cell Responses: An Under-Appreciated Partnership in Host Defence.Frontiers in immunology · 2021Review
- IL-33 facilitates rapid expulsion of the parasitic nematode Strongyloides ratti from the intestine via ILC2- and IL-9-driven mast cell activation.PLoS pathogens · 2020Article
- Cytokines and beyond: Regulation of innate immune responses during helminth infection.Cytokine · 2020Review
- Article
- Basophils and Eosinophils in Nematode Infections.Frontiers in immunology · 2020Review
- Role of mast cells in the generation of a T-helper type 2 dominated anti-helminthic immune response.Bioscience reports · 2019Article
- Sequential Changes in the Host Gut Microbiota During Infection With the Intestinal Parasitic NematodeFrontiers in cellular and infection microbiology · 2019Article
- Interleukin-9 promotes early mast cell-mediated expulsion of Strongyloides ratti but is dispensable for generation of protective memory.Scientific reports · 2018Article
- Nematode-Infected Mice Acquire Resistance to Subsequent Infection With Unrelated Nematode by Inducing Highly Responsive Group 2 Innate Lymphoid Cells in the Lung.Frontiers in immunology · 2018Article
- Differences in the Importance of Mast Cells, Basophils, IgE, and IgG versus That of CD4Infection and immunity · 2017Article
- IgE and mast cells in host defense against parasites and venoms.Seminars in immunopathology · 2016Review
- Roles and relevance of mast cells in infection and vaccination.Journal of biomedical research · 2016Review
- A single glycan on IgE is indispensable for initiation of anaphylaxis.The Journal of experimental medicine · 2015Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The host deploys a subset of immune responses to expel helminths, which differs depending on the nature of the helminth. Strongyloides venezuelensis, a counterpart of the human pathogen S. stercoralis, naturally infects rodents and has been used as an experimental model. Here we show that induction of immunoglobulin G (IgG) and IgE is a prerequisite for rapid expulsion of S. venezuelensis during a primary infection. Activation-induced cytidine deaminase-deficient (AID(-/-)) mice, which lack the ability to switch IgM to other isotypes, normally developed T-helper 2 (Th2) cells and intestinal mastocytosis after infection with S. venezuelensis. Although AID(-/-) mice expelled Nippostrongylus brasiliensis normally, they required a much longer period to expel S. venezuelensis than wild-type (WT) mice. Adoptive transfers of immune sera from S. venezuelensis-infected but not N. brasiliensis-infected mice restored the ability of AID(-/-) mice to promptly expel S. venezuelensis. Immune serum-derived IgG and IgE induced worm expulsion via Fc γ receptor III (FcγRIII) and Fc ε receptor I (FcεRI), respectively, and a mixture of IgG and IgE showed collaborative effects. Whereas FcγRIII(-/-) mice or FcεRIα(-/-) mice normally could expel S. venezuelensis, FcγRIII(-/-) mice, when their IgE was neutralized by anti-IgE, or FcεRIα(-/-) mice, when their IgG binding to FcγRIII was blocked by anti-FcγRIII, showed a markedly reduced ability to expel S. venezuelensis. These data reveal that IgG and IgE play redundant roles but act in concert to accelerate S. venezuelensis expulsion. Mast cell-deficient mice, even those equipped with immune serum-derived IgG or IgE, failed to expel S. venezuelensis promptly, suggesting that mast cells are cellular targets of IgG and IgE.
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