Deficiency in the glycosyltransferase Gcnt1 increases susceptibility to tuberculosis through a mechanism involving neutrophils.

doi:10.1038/s41385-020-0277-7

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Article

Deficiency in the glycosyltransferase Gcnt1 increases susceptibility to tuberculosis through a mechanism involving neutrophils.

Mucosal immunology - 1 Sept 2020

Fonseca Kaori L, Maceiras Ana Raquel, Matos Rita, Simoes-Costa Luisa, Sousa Jeremy, Cá Baltazar, Barros Leandro, Fernandes Ana Isabel, Mereiter Stefan, Reis Ricardo, Gomes Joana, Tapia Gustavo, Rodríguez-Martínez Paula, Martín-Céspedes Montse, Vashakidze Sergo, Gogishvili Shota, Nikolaishvili Keti, Appelberg Rui, Gärtner Fátima, Rodrigues Pedro N S, Vilaplana Cristina, Reis Celso A, Magalhães Ana, Saraiva Margarida

Abstract excerpt

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...

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Identifiers

PMID: 32203062
DOI: 10.1038/s41385-020-0277-7
PMCID: PMC7434595

Genes

CXCL2

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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