ArticleInfection and immunity2011
Modulation of early β-defensin-2 production as a mechanism developed by type I Toxoplasma gondii to evade human intestinal immunity.
Article in Infection and immunity, 2011. 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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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Evolution ofJournal of parasitology research · 2026Review
- Antimicrobial Peptides (AMPs): Potential Therapeutic Strategy against Trypanosomiases?Biomolecules · 2023Review
- ExploringFrontiers in cellular and infection microbiology · 2023Review
- Activity of Anti-Microbial Peptides (AMPs) againstBiomolecules · 2021Review
- Mycophenolic acid induces differentiation of Toxoplasma gondii RH strain tachyzoites into bradyzoites and formation of cyst-like structure in vitro.Parasitology research · 2018Article
- The P2X7 Receptor MediatesFrontiers in immunology · 2017Article
- Strain hypothesis of Toxoplasma gondii infection on the outcome of human diseases.Acta physiologica (Oxford, England) · 2015Review
- Antimicrobial Human β-Defensins in the Colon and Their Role in Infectious and Non-Infectious Diseases.Pathogens (Basel, Switzerland) · 2013Review
- Genome-wide analysis of peptidase content and expression in a virulent and attenuated Babesia bovis strain pair.Molecular and biochemical parasitology · 2011Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated the early innate immune responses induced in human intestinal epithelial cells (IEC) by the three defined Toxoplasma gondii genotype strains. Transcriptome analysis revealed that among differentially expressed genes, β-defensins distinguished the most IEC infected by fast- or slow-replicating T. gondii genotypes. Although β-defensin 1 and 3 genes were not expressed in host cells at early time points postinfection, the slow-replicating type II and III parasites induced high levels of β-defensin 2 gene expression. Notably, no β-defensin 2 gene expression occurred early after infection with the fast-replicating type I parasite. However, activation of this gene in IEC by poly(I:C) treatment prior to infection substantially decreased parasite viability, and pretreatment of parasites with synthetic β-defensin 2 significantly reduced their infectivity of IEC. These findings strongly support the modulation of early β-defensin 2 expression as a mechanism used by type I T. gondii parasites to mediate immune evasion.
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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.