L-selectin-mediated lymphocyte rolling on MAdCAM-1

Berg, Ellen L.; McEvoy, Leslie M.; Berlin, C; Bargatze, Robert F.; Butcher, Eugene C.

doi:10.1038/366695a0

Cited by 502 publications

(278 citation statements)

References 28 publications

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“…Both molecules have glycosyl phosphatidylinositol membrane anchors, but whether this has significance for rolling is unclear. Despite the ability of L-selectin to mediate rolling on carbohydrate ligands (17,18), mAbs DREG56 and DREG200 to L-selectin did not support rolling even when tested over a range of coating densities (not shown), implying that the ability to mediate rolling does not correlate to the structure or location of the cell surface antigen͞ receptor alone (16).…”

Section: Resultsmentioning

confidence: 99%

Rolling and transient tethering of leukocytes on antibodies reveal specializations of selectins

Chen

Alon

Fuhlbrigge

et al. 1997

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

110

111

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Antibodies immobilized on the wall of a flow chamber can support leukocyte rolling in shear flow. IgM mAb to Lewis x (CD15) and sialyl Lewis x (CD15s), which are carbohydrate antigens related to selectin ligands, plus mAb to CD48 and CD59, could mediate rolling. IgM and IgG mAb to L-selectin (CD62L), lymphocyte function-associated antigen 1 (CD11a), CD43, intercellular adhesion molecule 3 (CD50), and CD45 mediated only firm adhesion. In contrast to selectins, antibodies supported rolling only within a restricted range of site densities and wall shear stresses, outside of which firm adhesion or detachment occurred. When wall shear stress was increased, rolling velocity increased rapidly for antibodies but not for selectins. The kinetics of dissociation from the substrate of transiently tethered cells also increased more rapidly as a function of shear stress for antibodies than for selectins. These comparisons emphasize a number of remarkable features of selectins, including the lack of development of firm adhesion, and suggest that specialized molecular or cellular mechanisms must be required to explain their ability to support rolling over a wide range of environmental variables.In the first step in accumulation in inflammatory sites and homing to lymphoid tissues, circulating leukocytes tether to the vessel wall and then roll in response to hydrodynamic drag forces (1, 2). During rolling, the adhesive contact zone between the cell and the vessel is rapidly translated along the vessel wall. This requires the rapid breakage and formation of adhesive bonds and that the rate of bond formation keep up with the rate of bond breakage. Only certain adhesion molecules, including selectins, some integrins, and CD44 have been found to support rolling (1,(3)(4)(5). By contrast, many adhesion molecules, including integrins but not selectins, support another class of adhesion termed ''firm adhesion,'' which often involves cell spreading and cell migration.Thus far, little is known about the characteristics that determine whether adhesion molecules support rolling adhesion or firm adhesion. It has been hypothesized that fast bond dissociation and association rates are important for rolling (6), and measurements on P-selectin are consistent with this idea (7,8). However, the interaction of CD2 with lymphocyte function-associated 3 (9, 10) and binding of an IgE antibody to its antigen (11) have similar kinetics but do not appear to support rolling. Another factor that may be important is the effect of force on bond association and dissociation kinetics (12). The effect of force has been measured on the duration of transient tethers of cells to the vessel wall, which occurs at selectin densities below the minimum required to support rolling. The rate of dissociation of P-selectin tethers is increased only modestly by hydrodynamic force (8), which would contribute to the stability of rolling adhesions.To allow comparisons to be made between molecules that are and are not physiologically specialized for rolling, we have te...

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Section: Resultsmentioning

confidence: 99%

Rolling and transient tethering of leukocytes on antibodies reveal specializations of selectins

Chen

Alon

Fuhlbrigge

et al. 1997

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

110

111

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“…Finally, leukocytes bearing L-selectin can be captured by specific sialylated sulfated oligosaccharides such as sulfated isoforms of sialyl Lewis x (sLe x ) tetrasaccharides: NeuNAc␣2-3Gal␤1-4(Fuc␣1-3)GlcNac. Sulfated isoforms of sLe x decorate the vascular addressins GlyCAM-1, CD34, MAdCAM-1, Sgp 200 , and podocalyxin-like protein (14)(15)(16)(17)(18). As leukocytes roll along the endothelial cell surface, they are activated to express integrins that promote increased adhesion and spreading, the second phase of leukocyte extravasation (9,17,18).…”

mentioning

confidence: 99%

Modification of P-selectin glycoprotein ligand-1 with a natural killer cell-restricted sulfated lactosamine creates an alternate ligand for L-selectin

Andre¹

2000

Proceedings of the National Academy of Sciences

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Natural killer (NK) cells are components of the innate immune system that can recognize and kill virally infected cells, tumor cells, and allogeneic cells without prior sensitization. NK cells also elaborate cytokines (e.g., interferon-␥ and tumor necrosis factor-␣) and chemokines (e.g., macrophage inflammatory protein-1␣) that promote the acquisition of antigen-specific immunity. NK cell differentiation is accompanied by the cell surface expression of a mucin-like glycoprotein bearing an NK cell-restricted keratan sulfate-related lactosamine carbohydrate, the PEN5 epitope. Here, we report that PEN5 is a post-translational modification of P-selectin glycoprotein ligand-1 (PSGL-1). The PEN5 epitope creates on PSGL-1 a unique binding site for L-selectin, which is independent of PSGL-1 tyrosine sulfation. On the surface of NK cells, the expression of PEN5 is coordinated with the disappearance of L-selectin and the up-regulation of Killer cell Ig-like Receptors (KIR). These results indicate that NK cell differentiation is accompanied by the acquisition of a unique carbohydrate, PEN5, that can serve as part of a combination code to deliver KIR ؉ NK cells to specific tissues.

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“…The structural analysis of the binding site has revealed that the first immunoglobulin-like motif is important for the interaction with α 4 ß 7 integrin [11,50]. A subset of MAd-CAM-1 isolated from mesenteric lymph nodes or Peyer's patches can also interact with L-selectin, whereas MAdCAM-1 isolated from tumor necrosis factor (TNF)-α-stimulated cultured endothelioma cells cannot [6]. This indicates that a particular variant of MAdCAM-1 on HEV expresses a specific carbohydrate structure that supports the interaction with L-selectin [6].…”

Section: Lymphocyte Circulation and Cell Adhesion Molecules In The Immentioning

confidence: 99%

Expression of potential lymphocyte trafficking mediator molecules in the mammary gland

Nishimura

2003

Vet. Res.

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-The mammary gland performs a variety of immunological functions, including protecting itself from mastitis and protecting neonates from infectious agents. Several molecules that mediate lymphocyte trafficking in the immune system are also expressed in the mammary gland. This review is focused on the immunological function of these molecules, especially glycosylation-dependent cell adhesion molecule-1 (GlyCAM-1) and mucosal addressin cell adhesion molecule-1 (MAdCAM-1) in the mammary gland. GlyCAM-1 is expressed in the lactating mouse mammary gland. Endothelial cells produce this protein and secrete it into milk. The glycosylated modification of mammary gland GlyCAM-1 is different from that of the lymph nodes, and lacks the binding ability for L-selectin on lymphocytes. GlyCAM-1 in the mammary gland is not involved in lymphocyte migration, and probably has another function besides that of the lymph nodes. MAdCAM-1 is expressed on endothelial cells of small venules around mouse mammary lobules during lactation. This molecule has the ability to interact with α 4 ß 7 integrin on lymphocytes and mediates lymphocyte recruitment to the mammary gland. The density of ß 7 + /CD3 + T-cells is correlated with the density of the MAdCAM-1-stained area, suggesting that MAdCAM-1 may mediate the migration of these cells. In contrast, there is no relationship between MAdCAM-1 expression and the number of ß 7 + /c-IgA + B-cells, implying that some other factor is involved in lymphocyte migration to the mammary gland. Chemokines, such as IL-8, GRO-α, MCP-1, RANTES and MEC, have been detected in human and mouse mammary glands. Although little information is available, these molecules may contribute to lymphocyte migration to the mammary gland. mammary gland / mucosal-associated lymphoid tissue (MALT) / glycosylation-dependent cell adhesion molecule-1 (GlyCAM-1) / mucosal addressin cell adhesion molecule-1 (MAdCAM-1)

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L-selectin-mediated lymphocyte rolling on MAdCAM-1

Cited by 502 publications

References 28 publications

Rolling and transient tethering of leukocytes on antibodies reveal specializations of selectins

Rolling and transient tethering of leukocytes on antibodies reveal specializations of selectins

Modification of P-selectin glycoprotein ligand-1 with a natural killer cell-restricted sulfated lactosamine creates an alternate ligand for L-selectin

Expression of potential lymphocyte trafficking mediator molecules in the mammary gland

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