| First Author | Priatel JJ | Year | 2000 |
| Journal | Immunity | Volume | 12 |
| Issue | 3 | Pages | 273-83 |
| PubMed ID | 10755614 | Mgi Jnum | J:79167 |
| Mgi Id | MGI:2387354 | Doi | 10.1016/s1074-7613(00)80180-6 |
| Citation | Priatel JJ, et al. (2000) The ST3Gal-I sialyltransferase controls CD8+ T lymphocyte homeostasis by modulating O-glycan biosynthesis. Immunity 12(3):273-83 |
| abstractText | 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. |
