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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adhesion of lymphocytes to mouse brain endothelial cells was studied after treatment of the endothelium with 1000 U/ml gamma interferon (IFN-gamma) for 1 h to 2 days. Adhesion was not significantly different from controls after 1 h but at 4 h and thereafter, adhesion increased in a time-related manner. IFN-gamma also increased the expression of class II major histocompatibility complex (MHC) and murine intercellular adhesion molecule-1 (ICAM-1) molecules on the endothelial cells. The level of expression of class II MHC molecules was related to the length of exposure to IFN-gamma. MAb blocking studies suggested that class II molecules were responsible for the IFN-gamma-induced increase in lymphocyte-endothelial cell adhesion. Transfection of a murine lung endothelial cell line with cDNA for the class II MHC molecule also produced a significant increase in lymphocyte-endothelial cell adhesion, suggesting that the class II MHC molecule may have a role in adhesion which is distinct from antigen presentation.
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PMID:Modulation of adhesion of lymphocytes to murine brain endothelial cells in vitro: relation to class II major histocompatibility complex expression. 134 74

The regulation of extracellular matrix (ECM) protein receptor expression was followed in the human promonocytic cell line U937 before and after stimulation either with PMA or various cytokines implicated in monocytopoiesis. On undifferentiated U937 cells, alpha-chains of very late Ag (VLA)-4, VLA-5, and VLA-6 were constitutively expressed whereas alpha-chains of VLA-2 (alpha 2) and vitronectin receptor (alpha V) were not. Maturation of U937 cells with PMA resulted in a marked decrease in alpha 4 expression (25% of control by day 5), and a small but significant increase in the expression of alpha 2 and alpha v over 4 days of stimulation. Unstimulated U937 cells attached to fibronectin (FN) but not to laminin (LM), collagens I/IV-coated surfaces. After PMA stimulation, U937 cells exhibited enhanced adherence on FN and expressed the ability to adhere to LM. PMA stimulation also promoted U937 spreading both on FN and LM. Adhesion on FN all along the maturation pathway was specifically and totally inhibited by anti-alpha 5 mAb but not by anti-alpha 4 mAb. Anti-beta 1, anti-alpha 6, anti-alpha 2, and anti-alpha v mAb, as well as Tyr-Ile-Gly-Ser-Arg and Arg-Gly-Asp synthetic peptides from LM, had no effect on adhesion of PMA-stimulated cells on LM, implying that U937 cell adherence to LM is mediated through hitherto distinct receptors. In the presence of rIFN-gamma, differentiating U937 cells did not adhere to LM and lost the capacity to bind to FN. Loss of adhesion to FN was correlated with the concomitant decrease in the expression of alpha 4 and alpha 5 integrin subunits. In contrast, TGF-beta 1 mimicked most of the effects of PMA by enhancing the attachment of maturating U937 cells on FN through alpha 5 receptors and by promoting adherence to LM. TGF-beta 1 stimulation also promoted U937 cell spreading on both FN- and LM-coated surfaces. The data suggest that inflammatory cytokines such as IFN-gamma and TGF-beta 1 may be critically important in the homing of monocytic cells at sites of inflammation by modulating cell-surface expression of ECM receptors.
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PMID:IFN-gamma and transforming growth factor-beta 1 differently regulate fibronectin and laminin receptors of human differentiating monocytic cells. 153 26

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

Adhesion of hematopoietic cells to endothelial (En) cells plays an important role in their migration into extravascular tissue. This report characterizes the adhesion properties of naive splenocytes to syngeneic and allogeneic mouse brain microvascular endothelium isolated from the BALB/c or SJL/j mouse strains. Syngeneic adhesion reaches maximum levels by 60 min at 37 degrees C, but is more pronounced in the BALB/c system (mean adhesion = 10.7% +/- 1.0) compared to adhesion seen in the SJL/j (mean adhesion = 4.3% +/- 0.6). BALB/c, but not SJL/j adhesion, seems to be mediated, at least in part, by the interaction of CD11a/CD18 (lymphocyte function-associated antigen 1 (LFA-1] with one of its ligands, because BALB/c adhesion is partially inhibited when the assay is carried out either in the presence of chelating agents or with antibodies to the CD11a/CD18 molecule. Activation of the endothelium with recombinant interferon-gamma (rIFN-gamma), recombinant interleukin-1 alpha (rIL-1 alpha), and recombinant tumor necrosis factor-alpha (rTNF-alpha), enhances adhesion in both BALB/c and SJL/j. IFN-gamma and IL-1 alpha mediated adhesion enhancement is abrogated by antibodies to the CD11a/CD18 molecules in the BALB/c but not in the SJL/j system. The adhesion of splenocytes to mouse brain En clearly has unique properties, and whether or not the differences seen in the SJL/j system in any way influences its susceptibility to the autoimmune demyelinating disease, experimental autoimmune encephalitis, remains to be determined.
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PMID:Adhesion of splenocytes to brain microvascular endothelium in the BALB/c and SJL/j mouse systems. 168 52

Adhesion of lymphocytes to endothelial cells (EC) is the requisite first element in the multistep process of transmigration from blood across the postcapillary venules. Selective expression of cell adhesion molecules (CM) by microvascular EC in lymphoid organs (e.g., lymph nodes) and during tissue inflammation modulates this traffic in a site-directed manner. CAM synthesis by EC is regulated in turn by cytokines released in the local microenvironment. Studies done largely with human umbilical vein EC have implicated IL-1, IFN-gamma, and TNF-alpha as cytokines which promote leukocyte adhesion to EC. In the work reported here, the responses of cultured microvascular EC derived from macaque lymph nodes to IL-1beta, IL-2, IFN-gamma, and IL-4 were examined. Increases in lymphocyte adhesion after preculture of microvascular EC in IL-1beta or IFN-gamma were typically 2-to 4-fold above controls and comparable to those reported for human umbilical vein EC. IL-2 had no effect. In contrast, IL-4 markedly enhanced adhesion to microvascular EC. IL-4-induced adhesion was observed as early as 4 h after induction, plateaued by 24 h, was stable through 72 h of culture, but decayed to basal levels within 72 h after removal of IL-4 from the cultures. IL-1beta, but not IL-2 or IFN-gamma, synergistically enhanced the action of IL-4 on cultured microvascular EC to promote lymphocyte binding. Adhesion triggered in this manner required de novo protein synthesis. However, the avidity of IL-4-activated microvascular EC for lymphocytes, and analyses of kinetics, cation and temperature dependence, and/or lack of blockade with mAb to endothelial leukocyte adhesion molecule-1, intra-cellular adhesion molecule-1, and MECA-79 indicated that these CAM were not central to the phenomenon. To aid identification of the relevant CAM, mAb specific to IL-4-induced microvascular EC were produced. One of these, 6G10, blocked up to 90% of lymphocyte adhesion to IL-4-induced microvascular EC, immunoprecipitated an IL-4-induced cell-surface molecule of 110-kDa molecular mass, and reacted specifically with Chinese hamster ovary cells transfected with human vascular cell adhesion molecule-1. Our results suggest that IL-4 may have potent effects on lymphocyte recirculation in vivo.
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PMID:IL-4 acts synergistically with IL-1 beta to promote lymphocyte adhesion to microvascular endothelium by induction of vascular cell adhesion molecule-1. 169 65

Adhesion of lymphocytes to high endothelial venule (HEV) cells is the first step in the migration of these cells from blood into lymph nodes and Peyer's patches (PP). In the present study, we isolated and cultured HEV cells from PP of the rat and assessed their capacity to interact with lymphocytes. Flow cytometric analysis with a rat HEV-specific mAb KJ-4 revealed that greater than 90% of the cultured cells were stained by the antibody. Furthermore, confluent monolayers of PP HEV cells retained the capacity to support the adhesion of lymphocytes from spleen, thoracic duct, and lymph nodes but not binding of immature cells from thymus and bone marrow, which are deficient in cells capable of binding to HEV in vivo. In addition, intraepithelial lymphocytes that preferentially migrated into mucosal lymphoid tissues were also enriched in cells that adhered to the endothelial monolayers. The binding process required energy, was calcium-dependent, and could be inhibited by cytochalasin D, trypsin, and mixed glycosidase. Interestingly, pretreatment of PP HEV cells with rTNF, IFN-gamma, or granulocyte-macrophage CSF significantly increased the endothelial adhesiveness for thoracic duct lymphocytes in a time- and dose-dependent manner. In contrast, stimulation of lymphocytes with phorbol ester or TNF resulted in the rapid modulation of the surface expression of the PP homing receptor and decrease in lymphocyte binding to normal or TNF-stimulated HEV cells. The adhesion of lymphocytes to normal or cytokine-stimulated HEV cells can be blocked by pretreatment of lymphocytes, but not HEV cells, with the PP homing receptor-specific 1B.2.6 antibody. Taken together, these experiments provide strong evidence that the interaction between lymphocytes and cultured HEV cells are mediated by adhesive mechanisms that regulate lymphocyte entry into PP in vivo and that cytokines can promote HEV adhesiveness for lymphocytes through increased expression of organ-specific ligands on HEV cells.
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PMID:Lymphocyte adhesion to cultured Peyer's patch high endothelial venule cells is mediated by organ-specific homing receptors and can be regulated by cytokines. 212 24

LFA-1 and LFA-3 expression is absent or low on Burkitt's lymphoma cell lines and low on the EBV-transformed B cell line UD61. Incubation of cells of BL2 and of UD61 with various concentrations of IL-4 resulted in induction of LFA-1 and LFA-3 expression in a dose dependent fashion. This effect was already observed after 16 h of incubation whereas maximal expression was obtained after 72 h. Induction of LFA-1 and LFA-3 expression seemed to be specific for IL-4, because IL-1, IL-2, IL-3, IFN-alpha, IFN-gamma and a low m.w. B cell growth factor were ineffective. LFA-1 and LFA-3 induction by IL-4 was blocked specifically by an anti-IL-4 antiserum. Induction of LFA-1 expression by IL-4 was furthermore confirmed at the specific LFA-1 beta-chain mRNA level. IL-4 was unable to induce LFA-1 expression on EBV-transformed lymphoblastoid cell lines of two LFA-1-deficient patients. BL2 grows as single cells, but induction of LFA-1 and LFA-3 expression by IL-4 was insufficient to induce homotypic cell adhesions and required PMA as a second signal. PMA alone did not induce LFA-1 antigen expression and was unable to induce adhesions between BL2 cells in the absence of IL-4 in 22 h assays. Addition of PMA to BL2 cells that expressed LFA-1 Ag upon incubation with IL-4 resulted in aggregate formation within 30 min. Adhesions between BL2 cells induced by IL-4 in combination with PMA were blocked by anti-LFA-1 beta or anti-LFA-1 alpha-chains mAb. In addition, these mAbs dispersed preformed aggregates of BL2 cells. Our results indicate that IL-4 can induce the adhesion molecules LFA-1 and LFA-3 on B cell lines, but that an additional activation signal provided by PMA was required for the induction of homotypic cell adhesions.
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PMID:IL-4 induces LFA-1 and LFA-3 expression on Burkitt's lymphoma cell lines. Requirement of additional activation by phorbol myristate acetate for induction of homotypic cell adhesions. 254 69

Engagement of the TCR modulates the avidity of several receptors that play key roles in lymphocyte adhesion and/or signal transduction, including CD8, CD11a/CD18 (LFA-1), CD2, and several beta 1-integrins. Here, we investigated whether CD4+ T cells similarly undergo TCR-regulated adhesion to isolated MHC class II proteins through CD4. Strong adhesion of a number of CD4+ T cell clones to immobilized antigenic peptide/class II complexes was readily detectable. Adhesion to antigenic class II proteins was CD4 dependent and inhibited by pretreatment of T cells with the protein tyrosine kinase inhibitor herbimycin A, suggesting that adhesion requires TCR- and/or CD4-derived signal transduction. Treatment of T cells with anti-TCR Ab strongly increased subsequent adhesion to the extracellular matrix proteins, fibronectin and vitronectin, but, significantly, not to immobilized nonantigenic class II proteins. Suboptimal densities of antigenic peptide/class II complexes also activated adhesion of T cells to coimmobilized fibronectin or vitronectin, and this resulted in production of IFN-gamma to levels exceeding those stimulated by optimal densities of antigenic class II complexes alone. However, no augmentation of adhesion or cytokine secretion occurred when self or third party class II proteins were coimmobilized with antigenic class II complexes. The present results, therefore, suggest fundamental differences in the mechanism by which the TCR regulates coreceptor adhesion in CD4+ and CD8+ T cells.
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PMID:Murine CD4+ T cells undergo TCR-activated adhesion to extracellular matrix proteins but not to nonantigenic MHC class II proteins. 756 Oct 90

Adhesive interactions between lymphocytes and components of the extracellular matrix (ECM) within a wound environment play a crucial role in determining the inflammatory response following tissue injury. In fetal wounds the extracellular matrix is composed predominantly of hyaluronic acid. Within this environment the inflammatory reaction as a result of injury is minimal. We propose that this lack of an inflammatory cell response in the fetal wound is due to the high levels of hyaluronic acid within the ECM and the inability of lymphocytes to adhere to this matrix component. Therefore, we examined the adhesive properties of fetal lymphocytes to fibronectin, vitronectin, collagen types I, III, IV, V, and hyaluronic acid--ECM components involved in fetal and adult wound environments. Fetal lymphocytes from both spleen and thymus demonstrated significant binding capabilities to fibronectin, vitronectin, and collagen types I and III. No intrinsic binding capabilities were detected to hyaluronic acid. Adhesion was not affected by the addition of IL-1, IFN-gamma, or phorbol dibutyrate. The inability of lymphocytes to adhere to hyaluronic acid helps to explain the lack of inflammation found in fetal wounds and serves to demonstrate the importance of ECM-lymphocyte interactions in determining the inflammatory response during fetal wound healing.
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PMID:The extracellular matrix of the fetal wound: hyaluronic acid controls lymphocyte adhesion. 804 Nov 33

Adhesive interactions between murine cerebrovascular endothelial cells (EC) which comprise the blood-brain barrier (BBB) and myelin basic protein (MBP)-specific encephalitogenic T lymphocytes were investigated. Adhesion was assessed by measuring the percent attachment of 51Cr-labeled T cells to EC monolayers. The basal level adhesion (20-35%) was significantly up-regulated by treating EC with recombinant murine gamma interferon (IFN-gamma), interleukin-1 alpha (IL-1 alpha) and/or tumor necrosis factor-alpha (TNF alpha). The ability of these cytokines to modulate adhesion was dose- and time-dependent and could be detected as early as 1 h after treatment. The expression of intercellular adhesion molecule-1 (ICAM-1) by EC was examined by immunofluorescence staining and ELISA. Although all unstimulated EC cultures expressed ICAM-1, treatment of EC with the above cytokines dramatically up-regulated the level of ICAM-1 expression in a dose- and time-dependent fashion similar to that observed in the adhesion assays. Treatment of EC with transforming growth factor-beta 1 (TGF beta) down-regulated the level of T cell adhesion on untreated EC in a dose-dependent manner. Pretreatment of EC with TGF beta also partially inhibited the up-regulation of adhesion induced by IFN-gamma, IL-1 alpha and/or TNF alpha. TGF beta had no effect on the up-regulation of ICAM-1 expression induced by IFN-gamma, IL-1 alpha and/or TNF alpha. These results indicate that in addition to ICAM-1, other molecules may be involved in adhesion of encephalitogenic T cells to the EC comprising the cerebral vasculature.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cytokine-regulated adhesion between encephalitogenic T lymphocytes and cerebrovascular endothelial cells. 809 22


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