Abstract
T lymphocyte activation evokes distinct changes in cell surface O-glycans. CD8+ T cells undergo an elimination of sialic acid on core 1 O-glycans and an induction of core 2 O-glycans until either apoptotic death or differentiation into memory cells. We find that the ST3Gal-I sialyltransferase is required for core 1 O-glycan sialylation and its deficiency induces core 2 O-glycan biosynthesis. Apoptosis ensues with the loss of peripheral CD8+ T cells in the absence of immune stimulation. Cell surface ligation of the ST3Gal-I substrate CD43 recapitulates this phenotype by a caspase 3-independent mechanism. Control of core 1 O-glycan sialylation in T lymphocytes by ST3Gal-I comprises a homeostatic mechanism that eliminates CD8+ T cells by apoptosis while facilitating the production of viable CD8+ memory T cells.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Antigens, CD*
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Apoptosis
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Base Sequence
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CD8-Positive T-Lymphocytes / cytology
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CD8-Positive T-Lymphocytes / metabolism*
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Caspase 1 / metabolism
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Caspase Inhibitors
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Cytotoxicity, Immunologic
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Enzyme Activation
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Gene Expression Regulation
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Glycoproteins / metabolism
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Homeostasis
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Leukosialin
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Lymphocyte Activation
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Mice
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Molecular Sequence Data
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Mutagenesis
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Polysaccharides / biosynthesis*
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Sialoglycoproteins / metabolism
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Sialyltransferases / genetics
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Sialyltransferases / metabolism*
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Substrate Specificity
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beta-Galactoside alpha-2,3-Sialyltransferase
Substances
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Antigens, CD
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Caspase Inhibitors
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Glycoproteins
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Leukosialin
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Polysaccharides
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Sialoglycoproteins
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Spn protein, mouse
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Sialyltransferases
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Caspase 1
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beta-Galactoside alpha-2,3-Sialyltransferase
Associated data
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GENBANK/AF214028
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GENBANK/AF214029
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GENBANK/AF214030