Negative regulation of T-cell activation and autoimmunity by Mgat5 N-glycosylation

By M. Demetriou, M. Granovsky, S. Quaggin, J. Dennis. Nature, 2001

903 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/060687905f7e68971a8a03cae423691569dd7f7f

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. Gabriel A. Rabinovich
2. A. Varki
3. M. Toscano
4. D. Gabrilovich
5. M. Flögel
6. S. Dabelić
7. J. Dumić
8. E. Sotomayor

In Molecular Biology

1. Gabriel A. Rabinovich
2. A. Varki
3. M. Toscano
4. M. Flögel
5. S. Dabelić
6. J. Dumić
7. P. Park
8. Mark M. Davis

Citations in the corpus

• T-cell-antigen recognition and the immunological synapse (2003, background): “An important regulatory role for N -glycan synthesis in T-cell activation has recently been shown by Dennis and colleague”
• Protein-glycan interactions in the control of innate and adaptive immune responses (2008, background): “Notably, multivalent galectin-3–N-glycan lattices can limit TCR clustering at sites of immunological synapse and increase agonist threshold for TCR signaling, and thus they may contribute to T cell homeostasi”
• Immunosuppressive strategies that are mediated by tumor cells. (2007, background): “In addition, Demetriou and colleagues found that multivalent complexes composed of galectin-3 and specific N-glycans may restrict the lateral mobility of TCR complexes and restrain TCR-mediated signal transduction (139).”
• Human Decidual Natural Killer Cells Are a Unique NK Cell Subset with Immunomodulatory Potential (2003, background): “Galectin binding restricts TCR recruitment to the synapse by formation of a lattice resulting from its binding to tetraantennary N-glycosylated glycoproteins (58).”
• Mammalian glycosylation in immunity (2008, neutral): “GnT5-deficient mice have increased delayed-type hypersensitivity responses, increased susceptibility to experimental autoimmune encephalomyelitis (EAE) and increased glomerulonephritis that is associated with immune-complex depositio”
• Biological roles of glycans (2016, background): “The N-linked glycans on cell surface glycoproteins can have varying degrees of branching (597), and glycan branching is specifically upregulated in T cell activation (598), and in malignant transformation (599–604).”
• Glycosylation in cellular mechanisms of health and disease. (2006, background): “Loss of the GlcNAcT-V glycosyltransferase, for example, was found to induce coclustering of T cell receptors at the cell surface, reducing the threshold for immune activation and causing autoimmune disease (Demetriou et al., 2001).”
• Galectins as modulators of tumour progression (2005, background): “and can restrict T-cell receptor (TCR)-initiated signal transduction by forming multivalent complexes with glycans present on the TC”
• Galectin-3: an open-ended story. (2006, background): “Interestingly, mice deficient in Mgat5 show enhanced delaytype hypersensitivity and increased susceptibility to autoimmune disorders [51].”
• Turning 'sweet' on immunity: galectin–glycan interactions in immune tolerance and inflammation (2009, background): “Elegant work has shown that multivalent galectin 3–N-glycan complexes can limit TCR clustering by restricting lateral TCR movement within the plane of the membrane, thereby increasing agonist threshold for TCR signallin”
• Complex N-glycan number and degree of branching cooperate to regulate cell proliferation and differentiation. (2007, background): “Thus, Mgat5 / cells display reduced galectin-3 binding to complex N-glycans on the T cell receptor (TCR; Demetriou et al., 2001) as well as EGF receptor (EGFR) and TbRII in epithelial cells (Partridge et al., 2004).”