ArticlePLoS pathogens2023
Deficiency in Galectin-3, -8, and -9 impairs immunity to chronic Mycobacterium tuberculosis infection but not acute infection with multiple intracellular pathogens.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Interplay of autophagy and Th1/Th2-mediated macrophage polarization in host-pathogen dynamics.Frontiers in cellular and infection microbiology · 2025Pooled it
- A single-cell atlas of peripheral immunity suggests immune subset attrition during tuberculosis dissemination.The Journal of international medical research · 2026Article
- Abnormal Galectin Signaling in the Pathomechanisms of Placental Dysfunction in Gestational Diabetes Mellitus.International journal of molecular sciences · 2026Review
- Galectins: Role and Therapeutics in Diabetes and Diabetic Foot Ulcers.Biomolecules · 2026Review
- Regulated expression of galectins 1 and 3 IS associated with dysregulated T cell responses in pulmonary and pleural tuberculosis.Medical microbiology and immunology · 2025Article
- Mycobacterial phthiocerol dimycocerosate induces Galectin-3 upregulation to impair proinflammatory responses and favor immune evasion.International journal of biological macromolecules · 2025Article
- A Narrative Review on the Multifaceted Roles of Galectins in Host-Pathogen Interactions DuringInternational journal of molecular sciences · 2025Review
- Exploring the multilayered response of TB bacterium Mycobacterial tuberculosis to lysosomal injury.FEMS microbiology reviews · 2025Review
- Autophagy in mycobacterial infections: molecular mechanisms, host-pathogen interactions, and therapeutic opportunities.Frontiers in cellular and infection microbiology · 2025Review
- Phenothiazines enhance antibacterial activity of macrophage by inducing ROS and autophagy.Frontiers in immunology · 2025Article
- The role of galectins in the regulation of autophagy and inflammasome in host immunity.Seminars in immunopathology · 2024Review
- Exploring host-pathogen interactions in the Dictyostelium discoideum-Mycobacterium marinum infection model of tuberculosis.Disease models & mechanisms · 2024Review
- Increased Levels of Galectin-3 in Critical COVID-19.International journal of molecular sciences · 2023Article
- Role of pattern recognition receptors in sensingHeliyon · 2023Review
- Deficiency in Galectin-3, -8, and -9 impairs immunity to chronic Mycobacterium tuberculosis infection but not acute infection with multiple intracellular pathogens.PLoS pathogens · 2023Article
- Atg8ylation as a host-protective mechanism againstFrontiers in tuberculosis · 2023Article
Corrections and comments
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Authors and funding
20 authors at 6 institutions in 1 country.
Funding
Abstract
Macrophages employ an array of pattern recognition receptors to detect and eliminate intracellular pathogens that access the cytosol. The cytosolic carbohydrate sensors Galectin-3, -8, and -9 (Gal-3, Gal-8, and Gal-9) recognize damaged pathogen-containing phagosomes, and Gal-3 and Gal-8 are reported to restrict bacterial growth via autophagy in cultured cells. However, the contribution of these galectins to host resistance during bacterial infection in vivo remains unclear. We found that Gal-9 binds directly to Mycobacterium tuberculosis (Mtb) and Salmonella enterica serovar Typhimurium (Stm) and localizes to Mtb in macrophages. To determine the combined contribution of membrane damage-sensing galectins to immunity, we generated Gal-3, -8, and -9 triple knockout (TKO) mice. Mtb infection of primary macrophages from TKO mice resulted in defective autophagic flux but normal bacterial replication. Surprisingly, these mice had no discernable defect in resistance to acute infection with Mtb, Stm or Listeria monocytogenes, and had only modest impairments in bacterial growth restriction and CD4 T cell activation during chronic Mtb infection. Collectively, these findings indicate that while Gal-3, -8, and -9 respond to an array of intracellular pathogens, together these membrane damage-sensing galectins play a limited role in host resistance to bacterial infection.
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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.