ArticlePLoS pathogens2019
The lectin-specific activity of Toxoplasma gondii microneme proteins 1 and 4 binds Toll-like receptor 2 and 4 N-glycans to regulate innate immune priming.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Insight Into Inflammasome Signaling: Implications forFrontiers in immunology · 2020Pooled it
- HarnessingAnnals of medicine · 2026Review
- Clustering of host N-glycans by the microneme MIC1/4/6 complex licenses Toxoplasma rhoptry discharge.The EMBO journal · 2026Article
- When glycobiology meets inflammasome activation: Insights and implications.Journal of advanced research · 2026Review
- Recombinant Microneme Proteins MIC1 and MIC4 fromPathogens (Basel, Switzerland) · 2025Article
- Establishment of an ELISA for detecting oocyst-derivedFrontiers in veterinary science · 2025Article
- The microneme protein1 (MIC1) of Chinese 1 Toxoplasma regulates pyroptosis through the TLR4/NLRP3 pathway in macrophages.Parasites & vectors · 2024Article
- Sugar-Coated: Can Multivalent Glycoconjugates Improve upon Nature's Design?Journal of the American Chemical Society · 2024Review
- Construction and biological function ofZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Article
- Intestinal microbiota imbalance resulted by anti-Toxoplasma gondii immune responses aggravate gut and brain injury.Parasites & vectors · 2024Article
- The role of IFN-γ-mediated host immune responses in monitoring and the elimination of Toxoplasma gondii infection.International immunology · 2024Review
- Ultrastructural insights into the microsporidian infection apparatus reveal the kinetics and morphological transitions of polar tube and cargo during host cell invasion.PLoS biology · 2024Article
- Article
- Immunogenicity and protective efficacy of recombinant chimeric antigens based on surface proteins ofFrontiers in immunology · 2024Article
- Effects of a complex probiotic preparation, Fengqiang Shengtai and coccidiosis vaccine on the performance and intestinal microbiota of broilers challenged with Eimeria spp.Parasites & vectors · 2023Article
- Article
- Mining the Proteome ofAnimals : an open access journal from MDPI · 2022Review
- Intestinal immune responses to commensal and pathogenic protozoa.Frontiers in immunology · 2022Review
- Dominique Soldati-Favre: BringingFrontiers in cellular and infection microbiology · 2022Article
- The pathogenicity and virulence ofVirulence · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 4 countries.
Funding
Abstract
Infection of host cells by Toxoplasma gondii is an active process, which is regulated by secretion of microneme (MICs) and rhoptry proteins (ROPs and RONs) from specialized organelles in the apical pole of the parasite. MIC1, MIC4 and MIC6 assemble into an adhesin complex secreted on the parasite surface that functions to promote infection competency. MIC1 and MIC4 are known to bind terminal sialic acid residues and galactose residues, respectively and to induce IL-12 production from splenocytes. Here we show that rMIC1- and rMIC4-stimulated dendritic cells and macrophages produce proinflammatory cytokines, and they do so by engaging TLR2 and TLR4. This process depends on sugar recognition, since point mutations in the carbohydrate-recognition domains (CRD) of rMIC1 and rMIC4 inhibit innate immune cells activation. HEK cells transfected with TLR2 glycomutants were selectively unresponsive to MICs. Following in vitro infection, parasites lacking MIC1 or MIC4, as well as expressing MIC proteins with point mutations in their CRD, failed to induce wild-type (WT) levels of IL-12 secretion by innate immune cells. However, only MIC1 was shown to impact systemic levels of IL-12 and IFN-γ in vivo. Together, our data show that MIC1 and MIC4 interact physically with TLR2 and TLR4 N-glycans to trigger IL-12 responses, and MIC1 is playing a significant role in vivo by altering T. gondii infection competency and murine pathogenesis.
Indexed as
Identifiers
What OpenQuestion holds
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.