期刊
IMMUNITY
卷 15, 期 2, 页码 237-247出版社
CELL PRESS
DOI: 10.1016/S1074-7613(01)00188-1
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资金
- NCI NIH HHS [CA16885] Funding Source: Medline
- NIAID NIH HHS [AI 44453] Funding Source: Medline
- NIGMS NIH HHS [GM57411] Funding Source: Medline
Lymphocytes home to lymph nodes, using L-selectin to bind specific ligands on high endothelial venules (HEV). In vitro studies implicate GIcNAc-6-sulfate as an essential posttranslational modification for ligand activity. Here, we show that genetic deletion of HEC-GIcNAc6ST, a sulfotransferase that is highly restricted to HEV, results in the loss of the binding of recombinant L-selectin to the luminal aspect of HEV, elimination of lymphocyte binding in vitro, and markedly reduced in vivo homing. Reactivity with MECA 79, an adhesion-blocking mAb that stains HEV in lymph nodes and vessels in chronic inflammatory sites, is also lost from the luminal aspects of HEV. These results establish a critical role for HEC-GIcNAc6ST in lymphocyte trafficking and suggest it as an important therapeutic target.
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