ReviewFrontiers in immunology2014
Importance of Both Innate Immunity and Acquired Immunity for Rapid Expulsion of S. venezuelensis.
Review in Frontiers in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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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Who cites it
10 citing papers in PubMed, 34 citations in OpenAlex.
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- Nitric oxide in parasitic infections: a friend or foe?Journal of parasitic diseases : official organ of the Indian Society for Parasitology · 2022Review
- It's a hard knock life for some: Heterogeneity in infection life history of salmonids influences parasite disease outcomes.The Journal of animal ecology · 2021Article
- Venestatin from parasitic helminths interferes with receptor for advanced glycation end products (RAGE)-mediated immune responses to promote larval migration.PLoS pathogens · 2021Article
- Chitin and Its Effects on Inflammatory and Immune Responses.Clinical reviews in allergy & immunology · 2018Review
- Unique Action of Interleukin-18 on T Cells and Other Immune Cells.Frontiers in immunology · 2018Review
- IgE and mast cells in host defense against parasites and venoms.Seminars in immunopathology · 2016Review
- Vaccination against parasites - status quo and the way forward.Porcine health management · 2016Review
- Interleukin-1 Family Cytokines in Liver Diseases.Mediators of inflammation · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the first part of this review, we described the relevant roles of endogenous IL-33 for accumulation of ILC2 and eosinophils even in the lungs of Rag2(-/-) mice. Type II alveolar epithelial (ATII) cells express IL-33 in their nucleus and infection with Strongyloides venezuelensis induces IL-33 production by increasing the number of ATII cells possibly by the action of chitin. IL-33 from ATII cells induces ILC2 proliferation and at the same time activates them to produce IL-5 and IL-13, which in combination induce lung eosinophilic inflammation, aiding to expel infected worms in the lungs. In the second part, we showed that, although AID(-/-) mice normally develop Th2 cells and intestinal mastocytosis after infection with S. venezuelensis, they need adoptive transfers of immune sera from S. venezuelensis infected mice to obtain the capacity to promptly expel S. venezuelensis. Thus, intestinal nematode infection induces various Th2 immune responses (e.g., Th2 cell, ILC2, goblet cell hyperplasia, intestinal mastocytosis, smooth muscle cell contraction, local and systemic eosinophilia, and high serum level of IgE and IgG1). However, all of them are not necessary for rapid expulsion of intestinal nematodes. Instead, some combinations of Th2 immune responses are essentially required.
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