Since lipid rafts (high-order plasma membrane domains enriched in cholesterol and sphingomyelin [SM]) have been implicated in facilitating phagocytosis, we evaluated whether these ordered domains govern macrophages' ability to phagocytose C. neoformans.
First-pass extracted concept
lipid rafts
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Evidence Snippets
Lipid rafts serve as anchoring platforms for membrane proteins.
Lipid rafts and sphingolipid-induced protein scaffolds will be discussed as a membrane interface for lipid-controlled cell signaling.
Supporting Sources
Linked Claims
Lipid rafts are critical for facilitating FcγRIII-mediated phagocytosis of Cryptococcus neoformans by macrophages.
Cholesterol or sphingomyelin depletion causes deficient IgG-mediated phagocytosis of Cryptococcus neoformans.
Repletion with the raft-promoting sterol 7-dehydrocholesterol rescues phagocytic deficiency caused by membrane perturbation, whereas the raft-inhibiting sterol coprostanol decreases IgG-mediated phagocytosis.
Cholesterol or sphingomyelin depletion decreases FcRγ phosphorylation, while 7-dehydrocholesterol restores phosphorylation and coprostanol leaves phosphorylation comparable to unstimulated cells.
Lipid rafts and sphingolipid-induced protein scaffolds act as a membrane interface for lipid-controlled cell signaling.
Quoted textsource-backed
Lipid rafts and sphingolipid-induced protein scaffolds will be discussed as a membrane interface for lipid-controlled cell signaling.