ArticleJournal of immunology (Baltimore, Md. : 1950)2014
MyD88 signaling inhibits protective immunity to the gastrointestinal helminth parasite Heligmosomoides polygyrus.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. 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, 36 citations in OpenAlex.
- The Roles of Various Immune Cell Populations in Immune Response against Helminths.International journal of molecular sciences · 2023Review
- Targeting helminths: The expanding world of type 2 immune effector mechanisms.The Journal of experimental medicine · 2023Review
- Microbial regulation of intestinal motility provides resistance against helminth infection.Mucosal immunology · 2022Article
- Tissue-based IL-10 signalling in helminth infection limits IFNγ expression and promotes the intestinal Th2 response.Mucosal immunology · 2022Article
- Defining the early stages of intestinal colonisation by whipworms.Nature communications · 2022Article
- A protocol for generating germ-freeSTAR protocols · 2021Article
- Multiscale interactome analysis coupled with off-target drug predictions reveals drug repurposing candidates for human coronavirus disease.Scientific reports · 2021Article
- Integrative biology defines novel biomarkers of resistance to strongylid infection in horses.Scientific reports · 2021Article
- Article
- Development of caecaloids to study host-pathogen interactions: new insights into immunoregulatory functions of Trichuris muris extracellular vesicles in the caecum.International journal for parasitology · 2020Article
- The central adaptor molecule TRIF influences L. sigmodontis worm development.Parasitology research · 2019Article
- The relationships between faecal egg counts and gut microbial composition in UK Thoroughbreds infected by cyathostomins.International journal for parasitology · 2018Article
- Enteric helminth-induced type I interferon signaling protects against pulmonary virus infection through interaction with the microbiota.The Journal of allergy and clinical immunology · 2017Article
- Macrobiota - helminths as active participants and partners of the microbiota in host intestinal homeostasis.Current opinion in microbiology · 2016Review
- Tuft cells, taste-chemosensory cells, orchestrate parasite type 2 immunity in the gut.Science (New York, N.Y.) · 2016Article
- Cohabitation in the Intestine: Interactions among Helminth Parasites, Bacterial Microbiota, and Host Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2015Review
- Review
- Immunology in wild nonmodel rodents: an ecological context for studies of health and disease.Parasite immunology · 2015Review
- Cultivation of Heligmosomoides polygyrus: an immunomodulatory nematode parasite and its secreted products.Journal of visualized experiments : JoVE · 2015Article
- Analysis of gene-environment interactions in postnatal development of the mammalian intestine.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
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Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
Abstract
Helminth parasites remain one of the most common causes of infections worldwide, yet little is still known about the immune signaling pathways that control their expulsion. C57BL/6 mice are chronically susceptible to infection with the gastrointestinal helminth parasite Heligmosomoides polygyrus. In this article, we report that C57BL/6 mice lacking the adapter protein MyD88, which mediates signaling by TLRs and IL-1 family members, showed enhanced immunity to H. polygyrus infection. Alongside increased parasite expulsion, MyD88-deficient mice showed heightened IL-4 and IL-17A production from mesenteric lymph node CD4(+) cells. In addition, MyD88(-/-) mice developed substantial numbers of intestinal granulomas around the site of infection, which were not seen in MyD88-sufficient C57BL/6 mice, nor when signaling through the adapter protein TRIF (TIR domain-containing adapter-inducing IFN-β adapter protein) was also ablated. Mice deficient solely in TLR2, TLR4, TLR5, or TLR9 did not show enhanced parasite expulsion, suggesting that these TLRs signal redundantly to maintain H. polygyrus susceptibility in wild-type mice. To further investigate signaling pathways that are MyD88 dependent, we infected IL-1R1(-/-) mice with H. polygyrus. This genotype displayed heightened granuloma numbers compared with wild-type mice, but without increased parasite expulsion. Thus, the IL-1R-MyD88 pathway is implicated in inhibiting granuloma formation; however, protective immunity in MyD88-deficient mice appears to be granuloma independent. Like IL-1R1(-/-) and MyD88(-/-) mice, animals lacking signaling through the type 1 IFN receptor (i.e., IFNAR1(-/-)) also developed intestinal granulomas. Hence, IL-1R1, MyD88, and type 1 IFN receptor signaling may provide pathways to impede granuloma formation in vivo, but additional MyD88-mediated signals are associated with inhibition of protective immunity in susceptible C57BL/6 mice.
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