Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Appropriately activated mononuclear phagocytes mediate contact-dependent tumoricidal activity. Adhesion structures involved in contact-dependent tumor cytotoxicity have not been defined. The present study was aimed at identifying the adhesion structures involved in the tumoricidal activity of activated (IFN-gamma + LPS) human monocytes. Tumor cells of different histological origin were used as targets in a 48-hr cytolysis assay. Anti-CD18 (integrin beta 2 chain) monoclonal antibodies (MAbs) substantially (50-80%) inhibited human monocyte cytotoxicity. When the role of different a-chains was studied, anti-alpha L (CD11a, LFA1), anti-alpha M (CD11b, Mac-1) and anti-alpha X (CD11c, p150,95) caused marginal inhibition, but the effect of the 3 combined was comparable to that of anti-CD18. Anti-CD18 MAb did not affect the release of various cytotoxic molecules (e.g. TNF) by activated human monocytes. Activated monocytes showed augmented binding to target cells and anti-CD18 MAb inhibited the binding of resting and activated monocytes to tumor target cells. While IFN-gamma alone augmented expression of leukocyte integrins and LPS had no effect, the 2 activation signals, combined for optimal stimulation of tumoricidal activity, resulted in no appreciable increase in these leukocyte adhesion molecules, as assessed by flow cytometry. Our results suggest that the augmented CD18-dependent binding of activated monocytes on tumor cells depends mainly upon changes in the adhesive properties of these molecules rather than upon increased numbers on the cell surface. Anti-ICAM-1 MAb significantly reduced monocyte cytotoxicity on tumor cells, which is consistent with a role of the CD11/CD18 adhesion pathway. These results implicate "activated" leukocyte (beta 2) integrins (CD11/CD18) as important adhesion molecules in the contact-dependent tumoricidal activity of human monocytes.
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PMID:Involvement of leukocyte (beta 2) integrins (CD18/CD11) in human monocyte tumoricidal activity. 167 46

Expression of adhesion molecules on endothelial cells (EC) can be up-regulated or induced by cytokines. The aim of the present study was to investigate the effect of IL-4 on both the expression of adhesion molecules on EC and monocyte adhesion to EC. Flow cytometric analysis showed that VCAM-1 expression on EC was up-regulated after stimulation with IL-4 for 24 h, whereas the expression of E-selectin (formerly called endothelial leucocyte adhesion molecule-1 (ELAM-1)) was not enhanced, and that of intercellular adhesion molecule-1 (ICAM-1) only slightly. The adhesion of monocytes to EC increased to maximum values upon stimulation of EC with IL-4 for 24 h. Coating of monocytes with MoAb against the integrin beta 2-subunit (CD18) significantly inhibited their adhesion to IL-4-stimulated EC; maximal inhibition was found when monocytes were coated with anti-CD18 MoAb in combination with MoAb against CD49d (the alpha-chain of VLA-4), whereas no inhibition was found when monocytes were coated only with MoAb against CD49d. Monocyte adhesion was not significantly inhibited when IL-4-stimulated EC were coated with MoAbs against ICAM-1 or VCAM-1 alone or in combination. Adhesion of monocytes was inhibited to a greater extent when in addition to coating of monocytes with MoAb against CD18 the EC were coated with MoAb against VCAM-1. From these results we conclude that monocytes bind to IL-4-stimulated EC via interaction of CD11/CD18 molecules on the monocytes with an as yet unknown endothelial ligand, and interaction of VLA-4 on monocytes with VCAM-1 on EC.
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PMID:Increased adhesion of human monocytes to IL-4-stimulated human venous endothelial cells via CD11/CD18, and very late antigen-4 (VLA-4)/vascular cell adhesion molecule-1 (VCAM-1)-dependent mechanisms. 768 78

The final steps of lymphocyte differentiation occur in secondary lymphoid organs where B and T lymphocytes interact with the lymphoid microenvironment. Although numerous studies describe the interactions of murine lymphocytes with dendritic, follicular and other antigen presenting cells, little is known on the interactions between lymphocytes and reticular cells, an important cellular component of spleen stroma. In this work we describe the culturing of complete murine spleen stromas and of two cell lines, Sp-1 and Sp-2, identified as of possible reticular origin, and describe the adhesive interactions between murine lymphocytes and human lymphoid cells with murine spleen stromal cells. FACS analysis indicates that the Sp-1 cell line shows a single cell type expressing VCAM-1 and CD44 constitutively. They do not express any of the markers described for follicular cells, interdigitating cells, macrophages or endothelial cells. Our data suggests that these cells represent a population of spleen reticular cells. The Sp-2 cell line shows two phenotypically different cell types that grow in association. FACS analysis demonstrates that both cell types express VCAM-1 and CD44 constitutively, but that they can be differentiated by the expression of CD11b and FcR. These data suggest that the Sp-2 cell line is composed of one type of stromal cell growing over an adherent layer of reticular cells. Furthermore, analysis of the non-B non-T cell fraction prepared from murine spleen shows that approximately 30% of these cells correspond to the CD44/VCAM-1 double positive cells. Murine B and T cells adhere to the complete stromas and to Sp-1 and Sp-2 cell lines. Activation of B cells with LPS had no effect on binding while binding of T cells to complete stromas increased up to threefold after Con-A treatment. Adhesion of human lymphoblastoid Daudi cells to complete spleen stromas is blocked by an anti-(murine) VCAM-1 antibody but not by an antibody to the (human) integrin alpha 4 subunit, while adhesion to the Sp-1 and Sp-2 stromas is blocked by antibodies against both molecules. Also, adhesion of Ramos cells to Sp-2 stromas is inhibited by antibodies to the integrin alpha 4 subunit and to murine VCAM-1. Antibodies to other adhesion receptors such as the integrin beta 2 subunit, ICAM-1 or CD44 have no effect on human cell binding to these stromas. Our results suggest that we have isolated a fraction of splenic reticular cells and that these cells can be cultured as a distinct cell line. The finding that these cells express CD44 and VCAM-1 constitutively and use some of these molecules for lymphocyte binding suggests that spleen reticular cells may be involved in the regulation of normal lymphocyte traffic through the spleen.
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PMID:Spleen-derived stromal cells. Adhesion molecules expression and lymphocyte adhesion to reticular cells. 943 27

Cardiovascular diseases, including acute coronary syndrome (ACS), are the leading cause of death among humans. Adhesion proteins, owing to their involvement in the initiation and progression of atherosclerotic lesions, contribute to the progression of coronary disease and ACS occurrence. Considering ambiguosity of results reported to date, we decided to conduct a preliminary investigation of adhesion protein gene expression in ACS patients as well as in healthy subjects by making use of oligonucleotide microarray technology. Analysis of eight microarrays revealed ten upregulated genes differentiating between the two groups: intercellular adhesion molecule-2, platelet/endothelial cell adhesion molecule-1, zyxin, integrin-linked kinase, calcium and integrin binding protein-1 (calmyrin), integrin beta 2, integrin beta 3 (ITGB3), integrin beta 7, integrin alpha 2b, and selectin P ligand. The expression of ITGB3 was found to have been downregulated.
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PMID:Oligonucleotide microarray and QRT-PCR study of adhesion protein gene expression in acute coronary syndrome patients. 2030 90