ArticleThe Journal of experimental medicine2003
Multiple T cell subsets control Francisella tularensis LVS intracellular growth without stimulation through macrophage interferon gamma receptors.
Article in The Journal of experimental medicine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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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
56 citing papers in PubMed, 102 citations in OpenAlex.
- Immunopeptidomics reveals conserved and abundant Francisella tularensis proteins as immunogenic CD4 T cell antigens in mice.PLoS pathogens · 2026Article
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- Modulatory Role of ATG5 Protein in Immune Modulation During Experimental Tularemia.Microorganisms · 2026Article
- A modified mycobacterial growth inhibition assay for the functional assessment of vaccine-mediated immunity.NPJ vaccines · 2024Article
- IL-12p40 is essential but not sufficient for Francisella tularensis LVS clearance in chronically infected mice.PloS one · 2023Article
- Novel Transcriptional and Translational Biomarkers of Tularemia Vaccine Efficacy in a Mouse Inhalation Model: Proof of Concept.Microorganisms · 2021Article
- Host Immunity andMicroorganisms · 2021Review
- Artificially induced MAIT cells inhibit M. bovis BCG but not M. tuberculosis during in vivo pulmonary infection.Scientific reports · 2020Article
- Article
- Immune lymphocytes halt replication of Francisella tularensis LVS within the cytoplasm of infected macrophages.Scientific reports · 2020Article
- Vaccine-Mediated Mechanisms ControllingPathogens (Basel, Switzerland) · 2020Article
- CXCL16 Stimulates Antigen-Induced MAIT Cell Accumulation but Trafficking During Lung Infection Is CXCR6-Independent.Frontiers in immunology · 2020Article
- Host restriction of Escherichia coli recurrent urinary tract infection occurs in a bacterial strain-specific manner.PLoS pathogens · 2018Article
- Interleukin-18 Is Critical for Mucosa-Associated Invariant T Cell Gamma Interferon Responses to Francisella SpeciesInfection and immunity · 2018Article
- Vaccine-Mediated Mechanisms Controlling Replication ofFrontiers in cellular and infection microbiology · 2018Article
- Adaptive Immunity toFrontiers in cellular and infection microbiology · 2018Review
- Inflammasome-Independent NLRP3 Restriction of a Protective Early Neutrophil Response to Pulmonary Tularemia.PLoS pathogens · 2016Article
- MAIT cells promote inflammatory monocyte differentiation into dendritic cells during pulmonary intracellular infection.The Journal of experimental medicine · 2016Article
- AnFrontiers in cellular and infection microbiology · 2016Article
- Next Generation Vaccine Biomarkers workshop October 30-31, 2014--Ottawa, Canada.Human vaccines & immunotherapeutics · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A variety of data suggest that in vivo production of interferon (IFN)-gamma is necessary, but not sufficient, for expression of secondary protective immunity against intracellular pathogens. To discover specific IFN-gamma-independent T cell mediated mechanisms, we took advantage of an in vitro culture system that models in vivo immune responses to the intracellular bacterium Francisella tularensis live vaccine strain (LVS). LVS-immune lymphocytes specifically controlled 99% of the growth of LVS in wild-type murine bone marrow-derived macrophages. Surprisingly, LVS-immune lymphocytes also inhibited LVS intracellular growth by as much as 95% in macrophages derived from IFN-gamma receptor knockout (IFNgammaR KO) mice. CD8+ T cells, and to a lesser degree CD4+ T cells, controlled LVS intracellular growth in both wild-type and IFNgammaR KO macrophages. Further, a unique population of Thy1+alphabeta+CD4-CD8- cells that was previously suggested to operate during secondary immunity to LVS in vivo strongly controlled LVS intracellular growth in vitro. A large proportion of the inhibition of LVS intracellular growth in IFNgammaR KO macrophages by all three T cell subsets could be attributed to tumor necrosis factor (TNF) alpha. Thus, T cell mechanisms exist that control LVS intracellular growth without acting through the IFN-gamma receptor; such control is due in large part to TNF-alpha, and is partially mediated by a unique double negative T cell subpopulation.
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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.