ArticleJournal of immunology (Baltimore, Md. : 1950)2012
The Tim3-galectin 9 pathway induces antibacterial activity in human macrophages infected with Mycobacterium tuberculosis.
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 54 papers, 1 of them a synthesis that pooled it.
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
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.
- An Emerging Role of TIM3 Expression on T Cells in Chronic Kidney Inflammation.Frontiers in immunology · 2021Pooled it
- Galectin-9 signaling through TIM-3 is involved in neutrophil-mediated Gram-negative bacterial killing: an effect abrogated within the cystic fibrosis lung.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- Pathogenesis of Tuberculosis: Interplay Between Host Antituberculosis Immunity and Immune Evasion Strategies ofMedComm · 2026Review
- Expression and clinical significance of peripheral blood NK cell surface co-signaling molecules in active pulmonary tuberculosis patients.BMC infectious diseases · 2025Article
- The role of coinhibitory receptor-expressing non-T cells in inflammation and immunity: unsung heroes or peripheral players?Experimental & molecular medicine · 2025Review
- Identification of galectin-9 and its antibacterial function in Yellow River carp (Frontiers in immunology · 2025Article
- Regulatory Mechanisms of Co-Inhibitory Receptors in Tuberculosis Immunity: Implications for Therapeutic Targets.ImmunoTargets and therapy · 2025Review
- The interplay between hormonal vitamin D and lipopolysaccharide signaling on human neutrophil transcriptional responses.Frontiers in immunology · 2025Article
- Plasma galectin-9 relates to cognitive performance and inflammation among adolescents with vertically acquired HIV.AIDS (London, England) · 2024Article
- The rs11684747 and rs55790676 SNPs of ADAM17 influence tuberculosis susceptibility and plasma levels of TNF, TNFR1, and TNFR2.Frontiers in microbiology · 2024Article
- Control ofFrontiers in immunology · 2023Article
- The paradox of immune checkpoint inhibition re-activating tuberculosis.The European respiratory journal · 2022Review
- Cellular Senescence in Immunity against Infections.International journal of molecular sciences · 2022Review
- Tim-3/Galectin-9 signaling pathway is involved in the cytokine changes in mice with alveolar echinococcosis.Molecular biology reports · 2022Article
- Obesity-induced galectin-9 is a therapeutic target in B-cell acute lymphoblastic leukemia.Nature communications · 2022Article
- T-Cell Exhaustion inMicroorganisms · 2021Review
- Galectin-8 Senses Phagosomal Damage and Recruits Selective Autophagy Adapter TAX1BP1 To ControlmBio · 2021Article
- Serum levels of inhibitory costimulatory molecules and correlations with levels of innate immune cytokines in patients with pulmonary tuberculosis.The Journal of international medical research · 2021Article
- Sensing of mycobacterial arabinogalactan by galectin-9 exacerbates mycobacterial infection.EMBO reports · 2021Article
- SCARF1 promotes M2 polarization of Kupffer cells via calcium-dependent PI3K-AKT-STAT3 signalling to improve liver transplantation.Cell proliferation · 2021Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 4 countries.
Funding
Abstract
T cell Ig and mucin domain 3 (Tim3) is an inhibitory molecule involved in immune tolerance, autoimmune responses, and antiviral immune evasion. However, we recently demonstrated that Tim3 and Galectin-9 (Gal9) interaction induces a program of macrophage activation that results in killing of Mycobacterium tuberculosis in the mouse model of infection. In this study, we sought to determine whether the Tim3-Gal9 pathway plays a similar role in human pulmonary TB. We identified that pulmonary TB patients have reduced expression of Tim3 on CD14(+) monocytes in vivo. By blocking Tim3 and Gal9 interaction in vitro, we show that these molecules contribute to the control of intracellular bacterial replication in human macrophages. The antimicrobial effect was partially dependent on the production of IL-1β. Our results establish that Tim3-Gal9 interaction activates human M. tuberculosis -infected macrophages and leads to the control of bacterial growth through the production of the proinflammatory cytokine IL-1β. Data presented in this study suggest that one of the potential pathways activated by Tim3/Gal9 is the secretion of IL-1β, which plays a crucial role in antimicrobial immunity by modulating innate inflammatory networks.
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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.