ArticleThe Journal of experimental medicine2001
A critical role for interleukin 18 in primary and memory effector responses to Listeria monocytogenes that extends beyond its effects on Interferon gamma production.
Article in The Journal of experimental medicine, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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45 citing papers in PubMed, 127 citations in OpenAlex.
- Co-Formulation of Recombinant Porcine IL-18 Enhances the Onset of Immune Response in a NewVaccines · 2023Article
- LAMP2 regulates autophagy in the thymic epithelium and thymic stroma-dependent CD4 T cell development.Autophagy · 2023Article
- Listeria monocytogenes bacteremia mimicking the systemic metastasis of adrenal cancer: a case report.BMC infectious diseases · 2022Article
- Memory CD8Science advances · 2021Article
- Modifying bacterial flagellin to evade Nod-like Receptor CARD 4 recognition enhances protective immunity against Salmonella.Nature microbiology · 2020Article
- Th1 responses in vivo require cell-specific provision of OX40L dictated by environmental cues.Nature communications · 2020Article
- Interleukin-18 in Health and Disease.International journal of molecular sciences · 2019Review
- IFN-Gamma-Dependent and Independent Mechanisms of CD4⁺ Memory T Cell-Mediated Protection from Listeria Infection.Pathogens (Basel, Switzerland) · 2018Article
- T cell expression of IL-18R and DR3 is essential for non-cognate stimulation of Th1 cells and optimal clearance of intracellular bacteria.PLoS pathogens · 2017Article
- Memory CD8(+) T Cells: Innate-Like Sensors and Orchestrators of Protection.Trends in immunology · 2016Review
- Listeria monocytogenes and the Inflammasome: From Cytosolic Bacteriolysis to Tumor Immunotherapy.Current topics in microbiology and immunology · 2016Review
- Mechanisms of Memory T Cell Activation and Effective Immunity.Advances in experimental medicine and biology · 2015Review
- Memory-T-cell-derived interferon-γ instructs potent innate cell activation for protective immunity.Immunity · 2014Article
- IRAK-1 bypasses priming and directly links TLRs to rapid NLRP3 inflammasome activation.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Listeria monocytogenes Meningoencephalitis Mimicking Stroke in a Patient with Chronic Lymphocytic Leukemia.Neurology and therapy · 2013Article
- Early events regulating immunity and pathogenesis during Listeria monocytogenes infection.Trends in immunology · 2012Review
- Serum IL-18 is closely associated with renal tubulointerstitial injury and predicts renal prognosis in IgA nephropathy.Mediators of inflammation · 2012Article
- TIR8/SIGIRR is an Interleukin-1 Receptor/Toll Like Receptor Family Member with Regulatory Functions in Inflammation and Immunity.Frontiers in immunology · 2012Article
- Transient Receptor Potential Melastatin 2 (TRPM2) ion channel is required for innate immunity against Listeria monocytogenes.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- The unexpected link between infection-induced apoptosis and a TH17 immune response.Journal of leukocyte biology · 2011Review
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10 authors.
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No grant is acknowledged in the PubMed record.
Abstract
The stimulation of interferon (IFN)-gamma by interleukin (IL)-12 has been shown to provide protection from intracellular pathogens such as Listeria monocytogenes. Tumor necrosis factor (TNF) is also a major player in the resolution of Listeria infections and is suggested to have more global effects than can be explained by the induction of IFN-gamma alone. Since IL-18 synergizes with IL-12 to induce IFN-gamma production by natural killer and T helper (Th)1 cells, we determined its role in responses to Listeria. IL-18 appeared to be even more potent than either IL-12 or IFN-gamma for protection against this pathogen and IL-18 enhanced bacterial clearance in the complete absence of IFN-gamma. Indeed IL-18 was comparable to TNF in its ability to resolve the infection and showed a lowered protective capacity in the absence of TNF. Moreover, IL-18 induced macrophages to secrete both TNF and nitric oxide after a Listeria infection. IL-18 was also essential for optimal IFN-gamma production by antigen-specific T cells. Therefore, IL-18 operates via its effects on both the innate immune response, including macrophages, as well as on Th1 cells, to protect against Listeria.
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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.