ArticleInfection and immunity2003
Mice genetically deficient in immunoglobulin E are more permissive hosts than wild-type mice to a primary, but not secondary, infection with the filarial nematode Brugia malayi.
Article in Infection and immunity, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- Mast cells and IgE in defense against lethality of venoms: Possible "benefit" of allergy[].Allergo journal international · 2020Article
- Human susceptibility to social influence and its neural correlates are related to perceived vulnerability to extrinsic morbidity risks.Scientific reports · 2018Article
- Mast Cells and IgE can Enhance Survival During Innate and Acquired Host Responses to Venoms.Transactions of the American Clinical and Climatological Association · 2017Review
- IgE and mast cells in host defense against parasites and venoms.Seminars in immunopathology · 2016Review
- The Mast Cell-IgE Paradox: From Homeostasis to Anaphylaxis.The American journal of pathology · 2016Review
- Immunology of lymphatic filariasis.Parasite immunology · 2014Review
- A comprehensive, model-based review of vaccine and repeat infection trials for filariasis.Clinical microbiology reviews · 2013Review
- Immunopathogenesis of lymphatic filarial disease.Seminars in immunopathology · 2012Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary and secondary murine and human infections with Brugia malayi are characterized by substantial increases in levels of immunoglobulin E (IgE). To investigate whether this is necessary for worm clearance, IgE(-/-) mice were subjected to primary- and secondary-infection protocols. Following a primary infection, IgE(-/-) mice displayed a profound deficit in their ability to clear an intraperitoneal injection of L3 infective-stage larvae in comparison to wild-type counterparts and maintained substantial worm burdens as late as 10 weeks postinfection. Although viable adult parasites were recovered at this late time point from IgE(-/-) mice, the majority of the mice remained free of microfilariae. IgE(-/-) cohorts subjected to a secondary-infection protocol were able to clear the challenge inoculation in an accelerated manner, with kinetics similar to that observed in the wild-type animals. Analysis of the humoral response in IgE(-/-) mice following infection demonstrates a defect in IgG1 and IgG2a production, in addition to the expected lack of IgE. The IgG1 deficiency is no longer evident following a secondary infection. These data imply that deficiencies other than IgE production (i.e., IgG1 production) deficiency may be responsible for the increased permissiveness of IgE(-/-) mice as hosts following infection with B. malayi.
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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.