ArticleInfection and immunity2013
Participation of MyD88 and interleukin-33 as innate drivers of Th2 immunity to Trichinella spiralis.
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 23 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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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- From the bench to the clinic: basophils and type 2 epithelial cytokines of thymic stromal lymphopoietin and IL-33.Clinical & translational immunology · 2024Review
- "Every cell is an immune cell; contributions of non-hematopoietic cells to anti-helminth immunity".Mucosal immunology · 2022Review
- 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
- Cellular context of IL-33 expression dictates impact on anti-helminth immunity.Science immunology · 2020Article
- Changes in the Expression of TLR2 During the Intestinal Phase of Trichinellosis.Journal of veterinary research · 2020Article
- Modulation of TLR2 and TLR4 in Macrophages FollowingHelminthologia · 2018Article
- Immunity to gastrointestinal nematode infections.Mucosal immunology · 2018Review
- Host-Parasite Interactions Promote Disease Tolerance to Intestinal Helminth Infection.Frontiers in immunology · 2018Review
- Extracellular Vesicles from a Helminth Parasite Suppress Macrophage Activation and Constitute an Effective Vaccine for Protective Immunity.Cell reports · 2017Article
- TLR Specific Immune Responses against Helminth Infections.Journal of parasitology research · 2017Review
- Article
- Regulation of the host immune system by helminth parasites.The Journal of allergy and clinical immunology · 2016Review
- Impact of Helminth Infections and Nutritional Constraints on the Small Intestine Microbiota.PloS one · 2016Article
- Toll-Like Receptor Gene Expression during Trichinella spiralis Infection.The Korean journal of parasitology · 2015Article
- Review
- Integrated innate mechanisms involved in airway allergic inflammation to the serine protease subtilisin.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Crucial and diverse role of the interleukin-33/ST2 axis in infectious diseases.Infection and immunity · 2015Review
- Eosinophils mediate protective immunity against secondary nematode infection.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- IL-33/ST2 axis promotes mast cell survival via BCLXL.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Development of fatal intestinal inflammation in MyD88 deficient mice co-infected with helminth and bacterial enteropathogens.PLoS neglected tropical diseases · 2014Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Trichinella spiralis is a highly destructive parasitic nematode that invades and destroys intestinal epithelial cells, injures many different tissues during its migratory phase, and occupies and transforms myotubes during the final phase of its life cycle. We set out to investigate the role in immunity of innate receptors for potential pathogen- or danger-associated molecular patterns (PAMPs or DAMPs). Focusing on the MyD88-dependent receptors, which include Toll-like receptors (TLRs) and interleukin-1 (IL-1) family members, we found that MyD88-deficient mice expelled worms normally, while TLR2/4-deficient mice showed accelerated worm expulsion, suggesting that MyD88 was active in signaling pathways for more than one receptor during intestinal immunity. A direct role for PAMPs in TLR activation was not supported in a transactivation assay involving a panel of murine and human TLRs. Mice deficient in the IL-1 family receptor for the DAMP, IL-33 (called ST2), displayed reduced intestinal Th2 responses and impaired mast cell activation. IL-33 was constitutively expressed in intestinal epithelial cells, where it became concentrated in nuclei within 2 days of infection. Nuclear localization was an innate response to infection that occurred in intestinal regions where worms were actively migrating. Th2 responses were also compromised in the lymph nodes draining the skeletal muscles of ST2-deficient mice, and this correlated with increased larval burdens in muscle. Our results support a mechanism in which the immune system recognizes and responds to tissue injury in a way that promotes Th2 responses.
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Registered trials
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