2. Academic Validation
  3. The ST3Gal-I sialyltransferase controls CD8+ T lymphocyte homeostasis by modulating O-glycan biosynthesis

The ST3Gal-I sialyltransferase controls CD8+ T lymphocyte homeostasis by modulating O-glycan biosynthesis

  • Immunity. 2000 Mar;12(3):273-83. doi: 10.1016/s1074-7613(00)80180-6.
J J Priatel 1,  D Chui,  N Hiraoka,  C J Simmons,  K B Richardson,  D M Page,  M Fukuda,  N M Varki,  J D Marth
Affiliations

Affiliation

  • 1 Howard Hughes Medical Institute, the Glycobiology Research and Training Center, and Department of Cellular and Molecular Medicine, University of California, San Diego, La Jolla 92093, USA.
PMID: 10755614 DOI: 10.1016/s1074-7613(00)80180-6
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.

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