The vascular E-selectin binds to the leukocyte integrins CD11/CD18

Kotovuori, Pekka; Tontti, Eveliina; Pigott, Rod; Shepherd, Maura; Kiso, Makoto; Hasegawa, Akira; Renkonen, Risto; Nortamo, Pekka; Altieri, Dario C.; Gahmberg, Carl G.

doi:10.1093/glycob/3.2.131

Cited by 75 publications

(33 citation statements)

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“…[34][35][36] However, mouse L-selectin has been shown not to bind mouse E-selectin, making this an unlikely ligand in our study. 35 E-selectin ligand-1 (ESL-1), 37,38 CD66-nonspecific cross-reacting antigen, 39 CD43, 40 and ␤ 2 integrin 41,42 have all been proposed as potential ligands on leukocytes for E-selectin, although CD43 does not appear to support rolling and to our knowledge ␤ 2 integrin and CD66 are not down-regulated. Recently, a family of glycolipids, namely ␣2,3-sLe x glycosphingolipids, have also been shown to support E-selectin-dependent rolling.…”

Section: Discussionmentioning

confidence: 89%

A down-regulatable E-selectin ligand is functionally important for PSGL-1–independent leukocyte–endothelial cell interactions

Zanardo

Bonder

Hwang

et al. 2004

Blood

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P-selectin glycoprotein-1 (PSGL-1) supports P-selectin-dependent rolling in vivo and in vitro. However, controversy exists regarding the importance of PSGL-1-dependent and -independent E-selectin rolling. Using antibodies against PSGL-1 and PSGL-1 ؊/؊ mice, we demonstrated abolition of P-selectin-dependent rolling but only partial inhibition of E-selectinmediated rolling in the cremaster microcirculation following local administration of tumor necrosis factor ␣ (TNF-␣). In vitro studies demonstrated that binding of recombinant mouse E-selectin chimera to PSGL-1 ؊/؊ neutrophils was dramatically decreased in mice treated systemically but not locally with TNF-␣. Further, PSGL-1 blockade abolished E-selectindependent rolling in wild-type mice following systemic TNF-␣ administration but not local TNF-␣ administration. Together, these data support an E-selectin ligand present on PSGL-1 ؊/؊ neutrophils that is down-regulatable upon systemic but not local activation. To determine whether the PSGL-1-independent E-selectin ligand was physiologically important, we used a P-and E-selectin-dependent cutaneous contact hypersensitivity model. Binding studies showed no E-selectin ligand down-regulation in this model. The few cells that rolled on E-selectin ligand following PSGL-1 antibody administration or in PSGL-1 deficiency were sufficient to induce profound contact hypersensitivity. In conclusion, E-selectin mediates PSGL-1-dependent and independent rolling and the latter can be down-regulated by systemic activation and can replace PSGL-1 to support the development of

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Section: Discussionmentioning

confidence: 89%

A down-regulatable E-selectin ligand is functionally important for PSGL-1–independent leukocyte–endothelial cell interactions

Zanardo

Bonder

Hwang

et al. 2004

Blood

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“…The soluble E-selectin and VCAM-1 were produced by deletion of the transmembrane and cytoplasmatic domains of full-length protein. The proteins were expressed from the pGW 1 HG vector in Chinese hamster ovary cells and purified on mAb affinity columns, as described (33). The purified protein was detected by a specific ELISA (British Biotechnology Products) and shown to be biologically active in cell binding assays (32).…”

Section: Methodsmentioning

confidence: 99%

Rolling and adhesion of human tumor cells on vascular endothelium under physiological flow conditions.

Giavazzi¹,

Foppolo²,

Dossi³

et al. 1993

J. Clin. Invest.

206

157

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“…A molecule known as E-selectin ligand-1 (ESL-1) serves as an E-selectin ligand on mouse neutrophils (7), but it is not expressed on human neutrophils nor on human hematopoietic stem and progenitor cells (HSPCs) (8). Biochemical assays have indicated that the leukocyte β 2 integrins LFA-1 (lymphocyte function-associated antigen 1 or CD11a/ CD18) and MAC-1 (macrophage-1 antigen or CD11b/CD18) can serve as E-selectin ligands on human leukocytes (9). CD43 has also been implicated to be an E-selectin ligand on mouse neutrophils and activated T cells (10), and we have reported that CD43 on human T cells can bind E-selectin, but not P-selectin (11).…”

mentioning

confidence: 99%

G-CSF Induces Membrane Expression of a Myeloperoxidase Glycovariant that Operates as an E-selectin Ligand on Human Myeloid Cells

Silvescu

Sackstein

2014

Proc. Natl. Acad. Sci. U.S.A.

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The host defense response critically depends on the production of leukocytes by the marrow and the controlled delivery of these cells to relevant sites of inflammation/infection. The cytokine granulocyte-colony stimulating factor (G-CSF) is commonly used therapeutically to augment neutrophil recovery following chemo/ radiation therapy for malignancy, thereby decreasing infection risk. Although best known as a potent inducer of myelopoiesis, we previously reported that G-CSF also promotes the delivery of leukocytes to sites of inflammation by stimulating expression of potent E-selectin ligands, including an uncharacterized ∼65-kDa glycoprotein. To identify this ligand, we performed integrated biochemical analysis and mass spectrometry studies of G-CSF-treated primary human myeloid cells. Our studies show that this novel E-selectin ligand is a glycoform of the heavy chain component of the enzyme myeloperoxidase (MPO), a well-known lysosomal peroxidase. This specialized MPO glycovariant, referred to as "MPO-Eselectin ligand" (MPO-EL), is expressed on circulating G-CSF-mobilized leukocytes and is naturally expressed on blood myeloid cells in patients with febrile leukocytosis. In vitro biochemical studies show that G-CSF programs MPO-EL expression on human blood leukocytes and marrow myeloid cells via induction of N-linked sialofucosylations on MPO, with concomitant cell surface display of the molecule. MPO-EL is catalytically active and mediates angiotoxicity on human endothelial cells that express E-selectin. These findings thus define a G-CSF effect on MPO chemical biology that endows unsuspected functional versatility upon this enzyme, unveiling new perspectives on the biology of G-CSF and MPO, and on the role of E-selectin receptor/ligand interactions in leukocyte migration and vascular pathology.glycosylation | leukemia | hematopoietic stem cell transplantation

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The vascular E-selectin binds to the leukocyte integrins CD11/CD18

Cited by 75 publications

References 0 publications

A down-regulatable E-selectin ligand is functionally important for PSGL-1–independent leukocyte–endothelial cell interactions

A down-regulatable E-selectin ligand is functionally important for PSGL-1–independent leukocyte–endothelial cell interactions

Rolling and adhesion of human tumor cells on vascular endothelium under physiological flow conditions.

G-CSF Induces Membrane Expression of a Myeloperoxidase Glycovariant that Operates as an E-selectin Ligand on Human Myeloid Cells

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