Multiplicity of Glycosphingolipid-Enriched Microdomain-Driven Immune Signaling

Glycosphingolipids (GSLs), together with cholesterol, sphingomyelin (SM), and glycosylphosphatidylinositol (GPI)-anchored and membrane-associated signal transduction molecules, form GSL-enriched microdomains. These specialized microdomains interact in a manner with various immune receptors, affectin...

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Bibliographic Details
Published in:International journal of molecular sciences 2021-09, Vol.22 (17), p.9565
Main Authors: Yokoyama, Noriko, Hanafusa, Kei, Hotta, Tomomi, Oshima, Eriko, Iwabuchi, Kazuhisa, Nakayama, Hitoshi
Format: Article
Language:English
Subjects:
Animals
Antigen presentation
Antigen Presentation - immunology
Apoptosis
Apoptosis - immunology
Cholesterol
Cytokines
Enrichment
Epidermal growth factor
Glucagon
Glycosphingolipids
Glycosphingolipids - immunology
Glycosylphosphatidylinositol
Humans
Hydrogen bonds
Immunology
Insulin resistance
Intracellular
Intracellular signalling
Ligands
Lipid metabolism
Lipids
Membrane Microdomains - immunology
Membranes
Metabolism
Microscopy
Neutrophils
Pathogens
Phagocytes
Phagocytes - immunology
Phagocytosis
Phagocytosis - immunology
Phase transitions
Proteins
Review
Signal transduction
Signal Transduction - immunology
Sphingomyelin
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Summary:Glycosphingolipids (GSLs), together with cholesterol, sphingomyelin (SM), and glycosylphosphatidylinositol (GPI)-anchored and membrane-associated signal transduction molecules, form GSL-enriched microdomains. These specialized microdomains interact in a manner with various immune receptors, affecting immune receptor-mediated signaling. This, in turn, results in the regulation of a broad range of immunological functions, including phagocytosis, cytokine production, antigen presentation and apoptosis. In addition, GSLs alone can regulate immunological functions by acting as ligands for immune receptors, and exogenous GSLs can alter the organization of microdomains and microdomain-associated signaling. Many pathogens, including viruses, bacteria and fungi, enter host cells by binding to GSL-enriched microdomains. Intracellular pathogens survive inside phagocytes by manipulating intracellular microdomain-driven signaling and/or sphingolipid metabolism pathways. This review describes the mechanisms by which GSL-enriched microdomains regulate immune signaling.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms22179565