ArticlePLoS pathogens2013
Epstein Barr virus-induced 3 (EBI3) together with IL-12 negatively regulates T helper 17-mediated immunity to Listeria monocytogenes infection.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- AddaVax-Adjuvanted Inactivated Vaccine Confers Protection Against Listeria monocytogenes Challenge in Mice.Current microbiology · 2026Article
- Article
- Cytokine Storm Syndromes Associated with Epstein-Barr Virus.Advances in experimental medicine and biology · 2024Review
- The imbalance between Type 17 T-cells and regulatory immune cell subsets in psoriasis vulgaris.Frontiers in immunology · 2022Review
- Article
- Impact of Interleukin-27p28 on T and B Cell Responses during Toxoplasmosis.Infection and immunity · 2019Article
- Innate and Adaptive Immune Responses duringMicrobiology spectrum · 2019Article
- IL-27 confers a protumorigenic activity of regulatory T cells via CD39.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Interleukin-17D Promotes Pathogenicity During Infection by Suppressing CD8 T Cell Activity.Frontiers in immunology · 2019Article
- Lower level of IL‑35 and its reduced inhibition in Th17 cells in patients with bone marrow mononuclear cells Coombs test‑positive hemocytopenia.Molecular medicine reports · 2018Article
- Commensal Propionibacterium strain UF1 mitigates intestinal inflammation via Th17 cell regulation.The Journal of clinical investigation · 2017Article
- Epstein-Barr virus-induced gene 3 (EBI3) can mediate IL-6The Journal of biological chemistry · 2017Article
- Blockade of STAT3 in T Cells Inhibits Germinal Center Reactions against Intranasal Allergens.Biomolecules & therapeutics · 2016Article
- Dissecting CD8+ NKT Cell Responses to Listeria Infection Reveals a Component of Innate Resistance.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Modulation of Dendritic Cell Activation and Subsequent Th1 Cell Polarization by Lidocaine.PloS one · 2015Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Although the protective functions by T helper 17 (Th17) cytokines against extracellular bacterial and fungal infection have been well documented, their importance against intracellular bacterial infection remains unclear. Here, we investigated the contribution of Th17 responses to host defense against intracellular bacteria Listeria monocytogenes and found that Th17 cell generation was suppressed in this model. Unexpectedly, mice lacking both p35 and EBI3 cleared L. monocytogenes as efficiently as wild-type mice, whereas p35-deficient mice failed to do so. Furthermore, both innate cells and pathogen-specific T cells from double-deficient mice produced significantly higher IL-17 and IL-22 compared to wild-type mice. The bacterial burden in the liver of double-deficient mice treated with anti-IL-17 was significantly increased compared to those receiving a control Ab. Transfer of Th17 cells specific for listeriolysin O as well as administration of IL-17 and IL-22 significantly suppressed bacterial growth in p35-deficient mice, indicating the critical contribution of Th17 responses to host defense against the intracellular pathogen in the absence of IL-12 and proper Th1 responses. Our findings unveil a novel immune evasion mechanism whereby the intracellular bacteria exploit IL-27EBI3 to suppress Th17-mediated protective immunity.
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