期刊
IMMUNITY
卷 12, 期 3, 页码 273-283出版社
CELL PRESS
DOI: 10.1016/S1074-7613(00)80180-6
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资金
- NATIONAL CANCER INSTITUTE [R37CA033000] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL057345] Funding Source: NIH RePORTER
- NCI NIH HHS [R37CA33000] Funding Source: Medline
- NHLBI NIH HHS [P01HL 57345] Funding Source: Medline
T lymphocyte activation evokes distinct changes in cell surface O-glycans. CD8(+) T cells undergo an elimination of sialic acid on core 10-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 10-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 10-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.
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