CD44 is a physiological E-selectin ligand on neutrophils

Yoshio Katayama, Andrés Hidalgo, Jungshan Chang, Anna Peired, Paul S. Frenette

研究成果: 雜誌貢獻文章

133 引文 (Scopus)

摘要

The selectin family of adhesion molecules and their glycoconjugated ligands are essential for blood polymorphonuclear neutrophil (PMN) extravasation into inflammatory and infectious sites. However, E-selectin ligands on PMNs are not well characterized. We show here that CD44 immunopurified from G-CSF-differentiated 32D cells or from peripheral blood PMNs binds specifically to E-selectin. In contrast, CD44 extracted from bone marrow stromal or brain endothelial cell lines does not interact with E-selectin, suggesting cell-specific posttranslational modifications of CD44. PMN-derived CD44 binding activity is mediated by sialylated, α(1,3) fucosylated, N-linked glycans. CD44 enables slow leukocyte rolling on E-selectin expressed on inflamed endothelium in vivo and cooperates with P-selectin glycoprotein ligand-1 to recruit neutrophils into thioglycollate-induced peritonitis and staphylococcal enterotoxin A-injected skin pouch. CD44 extracted from human PMNs also binds to E-selectin. Moreover, we demonstrate that CD44 is hypofucosylated in PMNs from a patient with leukocyte adhesion deficiency type II, suggesting that it contributes to the syndrome. These findings thus suggest broader roles for CD44 in the innate immune response and uncover a potential new target for diseases in which selectins play a prominent role.

原文英語
頁(從 - 到)1183-1189
頁數7
期刊Journal of Experimental Medicine
201
發行號8
DOIs
出版狀態已發佈 - 四月 18 2005
對外發佈Yes

指紋

E-Selectin
Neutrophils
Ligands
Selectins
Leukocyte Rolling
Thioglycolates
Granulocyte Colony-Stimulating Factor
Post Translational Protein Processing
Peritonitis
Innate Immunity
Endothelium
Polysaccharides
Endothelial Cells
Bone Marrow
Cell Line
Skin
Brain

ASJC Scopus subject areas

  • Immunology

引用此文

CD44 is a physiological E-selectin ligand on neutrophils. / Katayama, Yoshio; Hidalgo, Andrés; Chang, Jungshan; Peired, Anna; Frenette, Paul S.

於: Journal of Experimental Medicine, 卷 201, 編號 8, 18.04.2005, p. 1183-1189.

研究成果: 雜誌貢獻文章

Katayama, Y, Hidalgo, A, Chang, J, Peired, A & Frenette, PS 2005, 'CD44 is a physiological E-selectin ligand on neutrophils', Journal of Experimental Medicine, 卷 201, 編號 8, 頁 1183-1189. https://doi.org/10.1084/jem.20042014
Katayama, Yoshio ; Hidalgo, Andrés ; Chang, Jungshan ; Peired, Anna ; Frenette, Paul S. / CD44 is a physiological E-selectin ligand on neutrophils. 於: Journal of Experimental Medicine. 2005 ; 卷 201, 編號 8. 頁 1183-1189.
@article{0ab24d6223e74a7193e5b7450eeb30bb,
title = "CD44 is a physiological E-selectin ligand on neutrophils",
abstract = "The selectin family of adhesion molecules and their glycoconjugated ligands are essential for blood polymorphonuclear neutrophil (PMN) extravasation into inflammatory and infectious sites. However, E-selectin ligands on PMNs are not well characterized. We show here that CD44 immunopurified from G-CSF-differentiated 32D cells or from peripheral blood PMNs binds specifically to E-selectin. In contrast, CD44 extracted from bone marrow stromal or brain endothelial cell lines does not interact with E-selectin, suggesting cell-specific posttranslational modifications of CD44. PMN-derived CD44 binding activity is mediated by sialylated, α(1,3) fucosylated, N-linked glycans. CD44 enables slow leukocyte rolling on E-selectin expressed on inflamed endothelium in vivo and cooperates with P-selectin glycoprotein ligand-1 to recruit neutrophils into thioglycollate-induced peritonitis and staphylococcal enterotoxin A-injected skin pouch. CD44 extracted from human PMNs also binds to E-selectin. Moreover, we demonstrate that CD44 is hypofucosylated in PMNs from a patient with leukocyte adhesion deficiency type II, suggesting that it contributes to the syndrome. These findings thus suggest broader roles for CD44 in the innate immune response and uncover a potential new target for diseases in which selectins play a prominent role.",
author = "Yoshio Katayama and Andr{\'e}s Hidalgo and Jungshan Chang and Anna Peired and Frenette, {Paul S.}",
year = "2005",
month = "4",
day = "18",
doi = "10.1084/jem.20042014",
language = "English",
volume = "201",
pages = "1183--1189",
journal = "Journal of Experimental Medicine",
issn = "0022-1007",
publisher = "Rockefeller University Press",
number = "8",

}

TY - JOUR

T1 - CD44 is a physiological E-selectin ligand on neutrophils

AU - Katayama, Yoshio

AU - Hidalgo, Andrés

AU - Chang, Jungshan

AU - Peired, Anna

AU - Frenette, Paul S.

PY - 2005/4/18

Y1 - 2005/4/18

N2 - The selectin family of adhesion molecules and their glycoconjugated ligands are essential for blood polymorphonuclear neutrophil (PMN) extravasation into inflammatory and infectious sites. However, E-selectin ligands on PMNs are not well characterized. We show here that CD44 immunopurified from G-CSF-differentiated 32D cells or from peripheral blood PMNs binds specifically to E-selectin. In contrast, CD44 extracted from bone marrow stromal or brain endothelial cell lines does not interact with E-selectin, suggesting cell-specific posttranslational modifications of CD44. PMN-derived CD44 binding activity is mediated by sialylated, α(1,3) fucosylated, N-linked glycans. CD44 enables slow leukocyte rolling on E-selectin expressed on inflamed endothelium in vivo and cooperates with P-selectin glycoprotein ligand-1 to recruit neutrophils into thioglycollate-induced peritonitis and staphylococcal enterotoxin A-injected skin pouch. CD44 extracted from human PMNs also binds to E-selectin. Moreover, we demonstrate that CD44 is hypofucosylated in PMNs from a patient with leukocyte adhesion deficiency type II, suggesting that it contributes to the syndrome. These findings thus suggest broader roles for CD44 in the innate immune response and uncover a potential new target for diseases in which selectins play a prominent role.

AB - The selectin family of adhesion molecules and their glycoconjugated ligands are essential for blood polymorphonuclear neutrophil (PMN) extravasation into inflammatory and infectious sites. However, E-selectin ligands on PMNs are not well characterized. We show here that CD44 immunopurified from G-CSF-differentiated 32D cells or from peripheral blood PMNs binds specifically to E-selectin. In contrast, CD44 extracted from bone marrow stromal or brain endothelial cell lines does not interact with E-selectin, suggesting cell-specific posttranslational modifications of CD44. PMN-derived CD44 binding activity is mediated by sialylated, α(1,3) fucosylated, N-linked glycans. CD44 enables slow leukocyte rolling on E-selectin expressed on inflamed endothelium in vivo and cooperates with P-selectin glycoprotein ligand-1 to recruit neutrophils into thioglycollate-induced peritonitis and staphylococcal enterotoxin A-injected skin pouch. CD44 extracted from human PMNs also binds to E-selectin. Moreover, we demonstrate that CD44 is hypofucosylated in PMNs from a patient with leukocyte adhesion deficiency type II, suggesting that it contributes to the syndrome. These findings thus suggest broader roles for CD44 in the innate immune response and uncover a potential new target for diseases in which selectins play a prominent role.

UR - http://www.scopus.com/inward/record.url?scp=18344376970&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=18344376970&partnerID=8YFLogxK

U2 - 10.1084/jem.20042014

DO - 10.1084/jem.20042014

M3 - Article

C2 - 15824084

AN - SCOPUS:18344376970

VL - 201

SP - 1183

EP - 1189

JO - Journal of Experimental Medicine

JF - Journal of Experimental Medicine

SN - 0022-1007

IS - 8

ER -