Glucosamine Modulates T Cell Differentiation through Down-regulating N-Linked Glycosylation of CD25*

@article{Chien2015GlucosamineMT,
  title={Glucosamine Modulates T Cell Differentiation through Down-regulating N-Linked Glycosylation of CD25*},
  author={Ming-Wei Chien and Ming-Hong Lin and Shing-Hwa Huang and Shin-Huei Fu and Chao-Yuan Hsu and B Linju Yen and Jiann-Torng Chen and Deh Ming Chang and Huey-Kang Sytwu},
  journal={The Journal of Biological Chemistry},
  year={2015},
  volume={290},
  pages={29329 - 29344}
}
Background: Glucosamine is an amino sugar that has immunoregulatory effects on T cell-mediated diseases. Results: Glucosamine inhibits Th1, Th2, iTreg cells, but promotes Th17 cell development through interference with N-glycosylation of CD25. Conclusion: Glucosamine modulates T cell differentiation in vivo and subsequently influences the progression and severity of autoimmune diseases. Significance: Glucosamine-mediated modulation of CD25 glycosylation can be beneficial to controlling… Expand
Glycans as Key Checkpoints of T Cell Activity and Function
TLDR
How specific glycans (with a focus on N-linked glycans) act as regulators of T cell biology and their implications in disease are discussed. Expand
The Modulatory Roles of N-glycans in T-Cell-Mediated Autoimmune Diseases
TLDR
This review summarizes and highlights the modulatory effects of N-glycosylation in several autoimmune diseases, including multiple sclerosis, systemic lupus erythematosus, inflammatory bowel disease, and type 1 diabetes mellitus. Expand
Glucosamine Interferes With Myelopoiesis and Enhances the Immunosuppressive Activity of Myeloid-Derived Suppressor Cells
Glucosamine (GlcN) is the most widely consumed dietary supplement and exhibits anti-inflammatory effects. However, the influence of GlcN on immune cell generation and function is largely unclear. InExpand
Glucosamine prevents polarization of cytotoxic granules in NK-92 cells by disturbing FOXO1/ERK/paxillin phosphorylation
TLDR
It is demonstrated that GlcN affects NK-92 cell cytotoxicity by altering the distribution of cathepsin C, a cysteine protease required for granzyme processing in cytotoxic granules, and it is elucidated that repositioning ofCatheps in C is a consequence of altered signaling pathways of cytot toxic granule movement. Expand
Melibiosamine, a novel oligosaccharide, suppresses mitogen-induced IL-2 production via inactivation of NFAT and NFκB in Jurkat cells
TLDR
It is found that GlcNH2 and MelNH2 at millimolar levels both significantly suppressed CIIP without affecting cell viability, suggesting that Mel NH2 may be a potentially useful lead compound for development as an immunosuppressive or anti-inflammatory drug. Expand
Pharmacologic inhibition of N-linked glycan trimming with kifunensine disrupts GLUT1 trafficking and glucose uptake.
TLDR
Results indicate that proper N-glycan processing plays an important role in directing GLUT1 to the cell surface and that disruption of mannosidase activity results in aberrant degradation ofGLUT1 by the ERAD pathway. Expand
Attenuated IL-2R signaling in CD4 memory T cells of T1D subjects is intrinsic and dependent on activation state.
TLDR
Results suggest that T1D-associated defects in the Teff compartment are due to intrinsic factors related to activation, and Evaluation of both Teff and Treg IL-2R signaling defects in T1d subjects may inform selection of therapies. Expand
Mechanism and effects of Zearalenone on mouse T lymphocytes activation in vitro.
TLDR
The results indicated that ZEA toxin interferes with the activation of mouse T lymphocytes by affecting TCR signal and co-stimulatory signal, thus playing an essential role in immune toxicity. Expand
Mathematical modeling of the early differentiation of helper T cells
TLDR
In this work, activation of naive CD4+ T cells under conditions of glutamine deprivation resulted in their differentiation to Foxp3+ regulatory T cells (Tregs), confirming that 'canonical' in vitro differentiation can be explained by a simple regulatory network. Expand
Re-Expression of Poly/Oligo-Sialylated Adhesion Molecules on the Surface of Tumor Cells Disrupts Their Interaction with Immune-Effector Cells and Contributes to Pathophysiological Immune Escape
TLDR
Re-expression of poly/oligo-sialylated adhesion molecules on the surface of tumor cells disrupts their interaction with immune-effector cells and contributes to pathophysiological immune escape, which can be the basis for future therapeutic intervention. Expand
...
1
2
3
...

References

SHOWING 1-10 OF 65 REFERENCES
N-Acetylglucosaminyltransferase V (Mgat5)-Mediated N-Glycosylation Negatively Regulates Th1 Cytokine Production by T Cells1
TLDR
Positive regulation of TCR signaling by β1,6GlcNAc N-glycans promotes development of Th2 over Th1 responses, enhances polarization of Th1 cells, and suggests a mechanism for the increased autoimmune disease susceptibility observed in Mgat5−/− mice. Expand
Control of T Cell-mediated Autoimmunity by Metabolite Flux to N-Glycan Biosynthesis*
TLDR
The results indicate that metabolite flux through the hexosamine and N-glycan pathways conditionally regulates autoimmunity by modulating multiple T cell functionalities downstream of β1,6GlcNAc-branched N- glycans, which suggests metabolic therapy as a potential treatment for autoimmune disease. Expand
Anti-cancer activity of glucosamine through inhibition of N-linked glycosylation
TLDR
The results suggested that the glucosamine-induced global inhibition of protein N-glycosylation might be the basic mechanism underlying its multiple biochemical and cellular effects. Expand
Negative regulation of T-cell activation and autoimmunity by Mgat5 N-glycosylation
TLDR
It is demonstrated that a deficiency in β1,6 N-acetylglucosaminyltransferase V (Mgat5), an enzyme in the N-glycosylation pathway, lowers T-cell activation thresholds by directly enhancing TCR clustering. Expand
Interleukin-2 at the crossroads of effector responses, tolerance, and immunotherapy.
TLDR
This review focuses on the molecular mechanisms and complex cellular actions of IL-2, its cooperative and opposing effects with other cytokines, and how both promoting and blocking the actions ofIL-2 are being utilized in clinical medicine. Expand
Immunosuppressive Effects of Glucosamine*
TLDR
The data demonstrate that glucosamine suppresses the activation of T-lymphoblasts and dendritic cells in vitro as well as allogeneic mixed leukocyte reactivity in a dose-dependent manner and could be beneficial as an immunosuppressive agent. Expand
Interleukin-2 signaling via STAT5 constrains T helper 17 cell generation.
TLDR
It is demonstrated that in addition to the promotion of activation-induced cell death of lymphocytes and the generation of Treg cells, inhibition of Th17 polarization appears to be an important function of IL-2. Expand
Glucosamine-induced OGT activation mediates glucose production through cleaved Notch1 and FoxO1, which coordinately contributed to the regulation of maintenance of self-renewal in mouse embryonic stem cells.
TLDR
GlcN-induced OGT activation mediated glucose production through cleaved Notch1 and FoxO1, which contributed to the regulation of maintenance of self-renewal in mESCs. Expand
Glucosamine Improved Atopic Dermatitis‐like Skin Lesions in NC/Nga Mice by Inhibition of Th2 Cell Development
TLDR
The production of Th2 cytokines, such as IL‐4 and IL‐5, was significantly decreased after in vitro administration of glucosamine, which suggest that glucosamines might be a useful immunomodulatory agent for the treatment of human AD. Expand
Regulation of Cytokine Receptors by Golgi N-Glycan Processing and Endocytosis
The Golgi enzyme β1,6 N-acetylglucosaminyltransferase V (Mgat5) is up-regulated in carcinomas and promotes the substitution of N-glycan with poly N-acetyllactosamine, the preferred ligand forExpand
...
1
2
3
4
5
...