Novel sulfated lymphocyte homing receptors and their control by a core1 extension β1,3-N-acetylglucosaminyltransferase

被引：287

作者：

Yeh, JC

Hiraoka, N

Petryniak, B

Nakayama, J

Ellies, LG

Rabuka, D

Hindsgaul, O

Marth, JD

Lowe, JB

Fukuda, M ^{[1
]}

机构：

[1] Burnham Inst, Ctr Canc Res, Glycobiol Program, La Jolla, CA 92037 USA

[2] Univ Michigan, Sch Med, Dept Pathol, Howard Hughes Med Inst, Ann Arbor, MI 48109 USA

[3] Shinshu Univ, Grad Sch Med, Inst Organ Transplants Reconstruct Med & Tissue E, Matsumoto, Nagano 3908621, Japan

[4] Univ Calif San Diego, Howard Hughes Med Inst, Div Cellular & Mol Med, La Jolla, CA 92093 USA

来源：

CELL | 2001年 / 105卷 / 07期

关键词：

D O I：

10.1016/S0092-8674(01)00394-4

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

L-selectin mediates lymphocyte homing by facilitating lymphocyte adhesion to addressins expressed in the high endothelial venules (HEV) of secondary lymphoid organs. Peripheral node addressin recognized by the MECA-79 antibody is apparently part of the L-selectin ligand, but its chemical nature has been undefined. We now identify a sulfated extended core1 mucin-type O-glycan, Gal beta1-->4(sulfo-->6)GlcNAc beta1-->3Gal beta1--> 3GalNAc, as the MECA-79 epitope. Molecular cloning of a HEV-expressed core1-beta1,3-N-acetylglucosaminyltransferase (Core1-beta 3GlcNAcT) enabled the construction of the 6-sulfo sialyl Lewis x on extended core1 O-glycans, recapitulating the potent L-selectin-mediated, shear-dependent adhesion observed with novel L-selectin ligands derived from core2 beta1,6-N-acetylglucosaminyltransferase-I null mice. These results identify Core1-beta 3GlcNAcT and its cognate extended core1 O-glycans as essential participants in the expression of the MECA-79-positive, HEV-specific L-selectin ligands required for lymphocyte homing.

引用

页码：957 / 969

页数：13

共 51 条

[1] Macular corneal dystrophy type I and type II are caused by distinct mutations in a new sulphotransferase gene [J].