Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.24.11 (CD10)
 9,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Leukocyte rolling precedes firm adhesion and emigration in inflammatory cell recruitment. Both P-selectin, an endothelial lectin that binds to sialylated O-glycans containing sialyl-Lewisx (sLex) on the granulocyte surface, and leukocyte L-selectin have been shown to mediate leukocyte rolling in vivo. Here, we investigate rolling of isolated human neutrophils (PMN), HL-60 promyelocytes, and an L-selectin-transfected cell line (300.19-L) during trauma-induced inflammation in rat mesenteric venules. HL-60 cells, which express no L-selectin but abundant sLex, rolled effectively immediately after abdominal surgery. HL-60 cell rolling was almost completely abolished by pretreatment with sialidase or monoclonal antibody (MoAb) AM-3 recognizing sLex, and was reduced by about 80% by O-sialoglycoprotein-endopeptidase (OSGP). By contrast, 300.19-L cells rolled poorly immediately after surgery but rolled well between 40 and 120 minutes after surgery. Their rolling was completely inhibited by the blocking L-selectin MoAb LAM1-3, but not by a binding control MoAb. PMN express both L-selectin and clustered, sialylated glycoproteins including P-selectin glycoprotein ligand-1 (PSGL-1). PMN showed effective rolling at all times, which was abolished by sialidase or MoAb AM-3 pretreatment during the first 30 minutes after surgery, but not later, when PMN rolling was largely L-selectin-dependent. We conclude that in trauma-induced inflammation, a two-step mechanism accounts for most of myeloid cell rolling, which initially requires O-glycans and subsequently depends on L-selectin function.
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PMID:Sialylated O-glycans and L-selectin sequentially mediate myeloid cell rolling in vivo. 754 70

We have compared the ability of human alpha/beta and gamma/delta T lymphocytes to adhere to selectin-bearing substrates, an interaction thought to be essential for homing and localization at sites of inflammation. Both T cell populations form rolling adhesions on E- and P-selectin substrates under physiologic flow conditions. Although equivalent to alpha/beta T cells in binding to E-selectin, gamma/delta T cells demonstrated greater ability to adhere to P-selectin that was purified or expressed on the surface of activated, adherent platelets. Under static conditions, 80% of gamma/delta T cells and 53% of alpha/beta T cells formed shear-resistant adhesions to P-selectin, whereas only 30% of gamma/delta and alpha/beta T cells adhered to E-selectin. The enhance ability of gamma/delta T cells to adhere to P-selectin cannot be attributed to differences in expression of the P-selectin glycoprotein ligand (PSGL-1), as all alpha/beta T cells versus approximately 75% of gamma/delta T cells expressed PSGL-1. Both cell populations expressed a similar percentage of the carbohydrate antigens sialyl LewisX and cutaneous lymphocyte-associated antigen. Depletion of lymphocyte populations or T cell clones bearing these oligosaccharides with the monoclonal antibody CSLEX-1 and HECA-452, respectively, resulted in a substantial reduction in adhesion to E-selectin and slight reduction in adhesion to P-selectin under flow conditions. Treatment of cells with an endopeptidase that selectively degrades O-sialomucins such as PSGL-1, abolished P-selectin but not E-selectin adhesion. Removal of terminal sialic acids with neuraminidase or protease treatment of cells abrogated cell adhesion to both selectin substrates. These results provide direct evidence for the presence of distinct E- and P-selectin ligands on T lymphocytes and suggest that gamma/delta T cells may be preferentially recruited to inflammatory sites during the early stages of an immune response when P-selectin is upregulated.
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PMID:Interactions of human alpha/beta and gamma/delta T lymphocyte subsets in shear flow with E-selectin and P-selectin. 864 61

The adhesive characteristics of hematopoietic stem and progenitor cells may partly regulate their proliferation and differentiation and may be critical in the homing of transplanted stem cells. Using quantitative adhesion assays, we have examined the characteristics of activated platelet adhesion to CD34+ cells in human blood and to the KG1a cell line. Approximately 85-95% of CD34+ cells from both sources bound thrombin-activated platelets; like mature neutrophils, activated platelet binding was maximal within 2 minutes of coincubation. Activated platelet adhesion to CD34+ cells was completely inhibited by chelation of calcium or by preincubation with the G1 blocking monoclonal antibody (MoAb) to platelet P-selectin. Using MoAbs to P-selectin glycoprotein ligand-1 (PSGL-1), we demonstrated that PSGL-1 was present on the surface of CD34+ cells; preincubation of CD34+ cells with the PL1 blocking MoAb to PSGL-1 completely inhibited activated platelet adhesion to CD34+ cells. Furthermore, treatment of CD34+ cells with O-sialoglycoprotein endopeptidase, which destroyed the PL1 epitope of PSGL-1, also abolished activated platelet-CD34+ cell binding. By contrast, MoAb directed against control epitopes of PSGL-1 or endopeptidase-sensitive epitopes of the CD34 molecule had no effect on activated platelet adhesion to CD34+ cells. Unlike mature neutrophils that, when activated, decrease P-selectin-dependent platelet adhesion because of redistribution of PSGL-1, phorbol ester treatment of CD34+ cells had no effect on their ability to bind activated platelets or PSGL-1 MoAbs. This study identifies PSGL-1 on CD34+ cells as the ligand for platelet P-selectin and suggests functional differences between mature and precursor hematopoietic cells in the regulation of surface PSGL-1 expression.
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PMID:Characterization of the P-selectin ligand on human hematopoietic progenitors. 895 Feb 32

Recirculation of B lymphocytes through the secondary lymphoid organs is key for recognition and response to foreign antigen. B lymphocytes within secondary lymphoid organs comprise a heterogeneous population of cells at distinct differentiation stages. To ascribe a particular adhesive behavior to discrete B-cell subsets within secondary lymphoid organs, we investigated their functional interaction with endothelial selectins under flow. We describe herein the characterization of a subset of human tonsillar B cells that interact with E-selectin but not P-selectin. E-selectin-interacting B cells had a phenotype of non-germinal center (CD10(-), CD38(-), CD44(+)), memory (IgD-) cells. Furthermore, FucT-VII was expressed selectively in CD44(+) E-selectin-adherent B lymphocytes. B-cell rolling on E-selectin required sialic acid but was independent of previously described selectin ligands. A novel glycoprotein ligand of 240 kDa carrying N-linked glycans was isolated from B-cell membranes by an E-selectin immunoadhesin. Binding of this protein was strictly Ca2+ dependent, was inhibited by a cell adhesion-blocking mAb against E-selectin, and required the presence of sialic acid but not N-linked carbohydrates. Our results enable us to assign to resident memory B lymphocytes a novel adhesion function, the rolling on E-selectin, that provides insights on the adhesion pathways involved in homing of memory B cells to tertiary sites.
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PMID:Memory B lymphocytes from secondary lymphoid organs interact with E-selectin through a novel glycoprotein ligand. 1022 75