3 results match your criteria: "Lipid Pathobiochemistry Group German Cancer Research Center[Affiliation]"
TLR9-mediated dendritic cell activation uncovers mammalian ganglioside species with specific ceramide backbones that activate invariant natural killer T cells.
PLoS Biol
March 2019
Univ. Lille, Centre d'Infection et d'Immunité de Lille, Lille, France.
Article Synopsis
- CD1d-restricted invariant natural killer T (iNKT) cells are a diverse group of immune cells that respond to lipid antigens, both from microbes and possibly from within the body (endogenous sources).
- The study identified two specific gangliosides (GM3 and GD3) as endogenous activators for mouse iNKT cells, showing that their activation relies on the structure of their ceramide backbone and the action of antigen-presenting cells.
- This research suggests that iNKT cells can quickly respond to changes in self-molecules during stress, offering insight into their role in immune responses and potential protective effects during bacterial infections.
Mammals synthesize, cell-type specifically, the diastereomeric hexosylceramides, β-galactosylceramide (GalCer) and β-glucosylceramide (GlcCer), which are involved in several diseases, such as sphingolipidosis, diabetes, chronic kidney diseases, or cancer. In contrast, , a member of the human gut microbiome, and the marine sponge, , produce α-GalCer, one of the most potent stimulators for invariant natural killer T cells. To dissect the contribution of these individual stereoisomers to pathologies, we established a novel hydrophilic interaction chromatography-based LC-MS method and separated ( > 1.
View Article and Find Full Text PDFZeb1 affects epithelial cell adhesion by diverting glycosphingolipid metabolism.
EMBO Rep
March 2015
Department of Cellular and Molecular Pathology, German Cancer Research Center (DKFZ), Heidelberg, Germany Sir William Dunn School of Pathology, University of Oxford, Oxford, UK
This study proposes that the transcription factor Zeb1 modulates epithelial cell adhesion by diverting glycosphingolipid metabolism. Zeb1 promotes expression of a-series glycosphingolipids via regulating expression of GM3 synthase (St3gal5), which mechanistically involves Zeb1 binding to the St3gal5 promoter as well as suppressing microRNA-mediated repression of St3gal5. Functionally, the repression of St3gal5 suffices to elevate intercellular adhesion and expression of distinct junction-associated proteins, reminiscent of knockdown of Zeb1.
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