ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Enhanced Tim3 activity improves survival after influenza infection.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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
20 citing papers in PubMed, 26 citations in OpenAlex.
- S1PR1 signaling biases neutrophils toward long-lived low-inflammatory functional states.bioRxiv : the preprint server for biology · 2026Article
- High-dimensional single-cell phenotyping unveils persistent differences in immune cell profiles between severe and moderate seasonal influenza.Frontiers in immunology · 2025Article
- Augmentation of Endothelial S1PR1 Attenuates Postviral Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2024Article
- Regulatory T cell-derived IL-1Ra suppresses the innate response to respiratory viral infection.Nature immunology · 2023Article
- Article
- Tim-3/Galectin-9 signaling pathway is involved in the cytokine changes in mice with alveolar echinococcosis.Molecular biology reports · 2022Article
- Notch4 signaling limits regulatory T-cell-mediated tissue repair and promotes severe lung inflammation in viral infections.Immunity · 2021Article
- Influenza infection, SARS, MERS and COVID-19: Cytokine storm - The common denominator and the lessons to be learned.Clinical immunology (Orlando, Fla.) · 2021Review
- Immune Checkpoints in Viral Infections.Viruses · 2020Review
- Glial TIM-3 Modulates Immune Responses in the Brain Tumor Microenvironment.Cancer research · 2020Article
- Dynamic Natural Killer Cell and T Cell Responses to Influenza Infection.Frontiers in cellular and infection microbiology · 2020Review
- Elevated neutrophil-to-lymphocyte ratio is an independent poor prognostic factor in patients with intrahepatic cholangiocarcinoma.Oncotarget · 2016Article
- Near Equilibrium Calculus of Stem Cells in Application to the Airway Epithelium Lineage.PLoS computational biology · 2016Article
- TIM-3 Suppresses Anti-CD3/CD28-Induced TCR Activation and IL-2 Expression through the NFAT Signaling Pathway.PloS one · 2015Article
- Regulation of T cell responses by the receptor molecule Tim-3.Immunologic research · 2014Review
- Increased frequency of Tim-3 expressing T cells is associated with symptomatic West Nile virus infection.PloS one · 2014Article
- Article
- Lung dendritic cells imprint T cell lung homing and promote lung immunity through the chemokine receptor CCR4.The Journal of experimental medicine · 2013Article
- Altering cell death pathways as an approach to cure HIV infection.Cell death & disease · 2013Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Influenza is a major cause of morbidity and mortality in the United States. Studies have shown that excessive T cell activity can mediate pneumonitis in the setting of influenza infection, and data from the 2009 H1N1 pandemic indicate that critical illness and respiratory failure postinfection were associated with greater infiltration of the lungs with CD8+ T cells. T cell Ig and mucin domain 3 (Tim3) is a negative regulator of Th1/Tc1-type immune responses. Activation of Tim3 on effector T cells has been shown to downregulate proliferation, cell-mediated cytotoxicity, and IFN-γ production, as well as induce apoptosis. In this article, we demonstrate that deletion of the terminal cytoplasmic domain of the Tim3 gene potentiates its ability to downregulate Tc1 inflammation, and that this enhanced Tim3 activity is associated with decreased phosphorylation of the TCR-CD3ζ-chain. We then show that mice with this Tim3 mutation infected with influenza are protected from morbidity and mortality without impairment in viral clearance or functional heterotypic immunity. This protection is associated with decreased CD8+ T cell proliferation and decreased production of inflammatory cytokines, including IFN-γ. Furthermore, the Tim3 mutation was protective against mortality in a CD8+ T cell-specific model of pneumonitis. These data suggest that Tim3 could be targeted to prevent immunopathology during influenza infection and demonstrate a potentially novel signaling mechanism used by Tim3 to downregulate the Tc1 response.
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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.