ArticleMucosal immunology2020
Deficiency in the glycosyltransferase Gcnt1 increases susceptibility to tuberculosis through a mechanism involving neutrophils.
Article in Mucosal immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02715271 (Study of TB Lesions Obtained in Surgery), which is not on this map. Cited by 18 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.
Study of TB Lesions Obtained in Surgery: in Search of Best Biomarkers Correlating With TB Pathology, Clinical Features, MDR Cases and Prognostic
Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
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- Pre-treatment blood cell counts and inflammatory markers predict the radiologic severity of post-tuberculosis lung disease.BMC infectious diseases · 2025Article
- Unravelling the transcriptome of the human tuberculosis lesion and its clinical implications.Nature communications · 2025Article
- Immunoinformatics Predictions on VariableMicroorganisms · 2025Article
- Enhancer RNA transcription pinpoints functional genetic variants linked to asthma.Nature communications · 2025Article
- Identification and functional characterization of glycosyltransferase-related biomarkers for tuberculosis diagnosis.AMB Express · 2025Article
- Activation of nuclear receptors correlates with tuberculosis severity and is a target for host-directed therapy.Frontiers in cellular and infection microbiology · 2025Article
- Genomic and ancestral variations linked to the development of post-acute sequelae of SARS-CoV-2 infection in Indian populations.Frontiers in genetics · 2025Article
- Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- Granulocytes subsets and their divergent functions in host resistance to Mycobacterium tuberculosis - a 'tipping-point' model of disease exacerbation.Current opinion in immunology · 2023Review
- Tirap controls Mycobacterium tuberculosis phagosomal acidification.PLoS pathogens · 2023Article
- SARS-CoV-2 variants induce distinct disease and impact in the bone marrow and thymus of mice.iScience · 2023Article
- Infection with hypervirulentFrontiers in immunology · 2023Article
- Association between lncRNA genetic variants and susceptibility to large artery atherosclerotic stroke.Metabolic brain disease · 2021Article
- Regulatory mechanisms of neutrophil migration from the circulation to the airspace.Cellular and molecular life sciences : CMLS · 2021Review
- Article
- Adhesion ofFrontiers in molecular biosciences · 2021Review
Corrections and comments
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Authors and funding
24 authors at 4 institutions in 3 countries.
Funding
Abstract
Modulation of immunity and disease by glycans is increasingly recognized. However, how host glycosylation shapes and is shaped by tuberculosis remains poorly understood. We show that deficiency in the glucosaminyl (N-acetyl) transferase 1 (Gcnt1), a key enzyme for core-2 O-glycans biosynthesis, drives susceptibility to Mycobacterium tuberculosis infection. The increased susceptibility of Gcnt1 deficient mice was characterized by extensive lung immune pathology, mechanistically related to neutrophils. Uninfected Gcnt1 deficient mice presented bone marrow, blood and lung neutrophilia, which further increased with infection. Blood neutrophilia required Gcnt1 deficiency in the hematopoietic compartment, relating with enhanced granulopoiesis, but normal cellular egress from the bone marrow. Interestingly, for the blood neutrophilia to translate into susceptibility to M. tuberculosis infection, Gnct1 deficiency in the stroma was also necessary. Complete Gcnt1 deficiency associated with increased lung expression of the neutrophil chemoattractant CXCL2. Lastly, we demonstrate that the transcript levels of various glycosyltransferase-encoding genes were altered in whole blood of active tuberculosis patients and that sialyl Lewis x, a glycan widely present in human neutrophils, was detected in the lung of tuberculosis patients. Our findings reveal a previously unappreciated link between Gcnt1, neutrophilia and susceptibility to M. tuberculosis infection, uncovering new players balancing the immune response in tuberculosis.
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Registered trials
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