The DOI matches its Crossref record; 52 of the 52 references it cites were found in a registry or an index.
Differential glycosylation of TH1, TH2 and TH-17 effector cells selectively regulates susceptibility to cell death
Abstract
Regulated glycosylation controls T cell processes, including activation, differentiation and homing by creating or masking ligands for endogenous lectins. Here we show that stimuli promoting T helper type 1 (TH1), TH2 or interleukin 17-producing T helper (TH-17) differentiation can differentially regulate the glycosylation pattern of T helper cells and modulate their susceptibility to galectin-1, a glycan-binding protein with anti-inflammatory activity. Although TH1- and TH-17-differentiated cells expressed the repertoire of cell surface glycans critical for galectin-1-induced cell death, TH2 cells were protected from galectin-1 through differential sialylation of cell surface glycoproteins. Consistent with those findings, galectin-1-deficient mice developed greater TH1 and TH-17 responses and enhanced susceptibility to autoimmune neuroinflammation. Our findings identify a molecular link among differential glycosylation of T helper cells, susceptibility to cell death and termination of the inflammatory response.
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“Of note, the glycosylation state of some death receptors (e.g., FAS) has been shown to impact on the sensitivity of T lymphocytes to extrinsic apoptosis, hence influencing the termination of inflammatory responses [288–290].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [288]
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A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17
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IL-23 drives a pathogenic T cell population that induces autoimmune inflammation
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Transforming growth factor-β induces development of the TH17 lineage
Mangan, P. R., Harrington, L. E., O'Quinn, D. B., Helms, W. S., Bullard, D. C., Elson, C. O., Hatton, R. D., Wahl, S. M., Schoeb, T. R., & Weaver, C. T. (2006) · Nature · doi:10.1038/nature04754 · Cited by 3,087
The Tim-3 ligand galectin-9 negatively regulates T helper type 1 immunity
Zhu, C., Anderson, A. C., Schubart, A., Xiong, H., Imitola, J., Khoury, S. J., Zheng, X. X., Strom, T. B., & Kuchroo, V. K. (2005) · Nature Immunology · doi:10.1038/ni1271 · Cited by 2,057
Anti-Inflammatory Activity of Immunoglobulin G Resulting from Fc Sialylation
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TH-17 cells in the circle of immunity and autoimmunity
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Interleukin-2 Signaling via STAT5 Constrains T Helper 17 Cell Generation
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Turning 'sweet' on immunity: galectin–glycan interactions in immune tolerance and inflammation
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Self-citation
Metadata
- Authors
- Toscano, M. A., Bianco, G. A., Ilarregui, J. M., Croci, D. O., Correale, J., Hernandez, J. D., Zwirner, N. W., Poirier, F., Riley, E. M., Baum, L. G., & Rabinovich, G. A.
- Affiliations
- Universidad de Buenos Aires (AR)
- Consejo Nacional de Investigaciones Científicas y Técnicas (AR)
- University of California, Los Angeles (US)
- London School of Hygiene & Tropical Medicine (GB)
- Corresponding author
- Rabinovich, Gabriel A
- ORCID
- Venue
- Nature Immunology
- Published
- 2007-06-24
- Volume
- 8
- Issue
- 8
- Pages
- 825-834
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- OpenAlex
- W2041659209
- Cited by
- 653
- References
- 52
- Citations by year
- 2026: 22 · 2025: 28 · 2024: 22 · 2023: 22 · 2022: 46 · 2021: 31 · 2020: 35 · 2019: 20 · 2018: 36 · 2017: 25 · 2016: 33 · 2015: 36 · 2014: 37 · 2013: 34 · 2012: 40
- FWCI
- 18.17
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Funders
- Wellcome Trust
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Glycosylation and Glycoproteins Research
- Life Sciences › Immunology and Microbiology › Immunology › Galectins and Cancer Biology
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- galectin-1, T helper cell differentiation, Th1 cells, Th2 cells, Th17 cells, sialylation, cell death, cell surface glycans, lectin binding, autoimmune neuroinflammation
- MeSH terms
- Animals, Cell Differentiation, Encephalomyelitis, Autoimmune, Experimental, Flow Cytometry, Glycosylation, T-Lymphocytes, Helper-Inducer, Humans, Inflammation, Membrane Glycoproteins, Polysaccharides, Immunoblotting, T-Lymphocyte Subsets, Apoptosis, Th1 Cells, Th2 Cells, Adoptive Transfer, In Situ Nick-End Labeling, Interleukin-17, Galectin 1, Mice
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