On the potential involvement of CD11d in co-stimulating the production of interferon- by natural killer cells upon interaction with neutrophils via intercellular adhesion molecule-3
Claudio CostantiniAlessandra MichelettiF. CalzettiOmar PerbelliniNicola TamassiaCristina AlbanesiWilliam VermiMarco A. Cassatella
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Interaction between neutrophils and other leukocytes plays a variety of important roles in regulating innate and adaptive immune responses. Recently, we have shown that neu-trophils amplify NK cell/6-sulfo LacNAc(+) dendritic cells (slanDC)-mediated cytokine production, by potentiating IL-12p70 release by slanDC via CD18/ICAM-1 and directly co-stimulating IFNγ production by NK cells via ICAM-3. Herein, we have identified additional molecules involved in the interactions among neutrophils, NK cells and slanDC. More specifically, we provide evidence that: i) the cross-talk between neutrophils and NK cells is mediated by ICAM-3 and CD11d/CD18, respectively; ii) slanDC potentiate the production of IFNγ by NK cells via CD11a/CD18. Altogether, our studies shed more light on the role that adhesion molecules play within the neutrophil/NK cell/slanDC network. Our data also have potential implications in the pathogenesis of diseases driven by hyperactivated leukocytes, such as Sweet's syndrome, in which a neutrophil/NK cell co-localization is frequently observed.Keywords:
CD11a
Abstract Both human integrin receptors Mac-1 (CD11b/CD18, CR3) and lymphocyte function-associated antigen (LFA)-1 (CD11a/CD18) have been demonstrated to bind human intercellular adhesion molecule-1 (ICAM-1) (CD54). Here we show that LFA-1 and Mac-1 can bind to ICAM-1 in the mouse as well. Interestingly, we observed that binding of murine LFA-1 dominates over Mac-1 for binding to ICAM-1. Using three different murine macrophage cell lines that express distinct levels of LFA-1 and Mac-1 on their cell surface, we could only detect Mac-1-dependent adhesion to ICAM-1 when little or no LFA-1 is expressed on the cell surface. When LFA-1 and Mac-1 are expressed at similar levels, the LFA-1/ICAM-1 interaction dominates over Mac-1/ICAM-l interaction, indicating that there is a competition of LFA-1 and Mac-1 for ICAM-1 binding.
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Intercellular adhesion molecule
Cell–cell interaction
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Bovine leukocyte adhesion deficiency (BLAD) was identified in a two-month-old Holstein heifer calf using DNA-polymerase chain reaction analysis of the affected calf and other clinical parameters. Neutrophil integrin expression (CD18, CD11a, CD11c), aggregation, and transendothelial migration were studied in vitro. Neutrophils were isolated from the affected calf and from normal, healthy, age-matched control Holstein calves. Neutrophils isolated from the affected BLAD calf had decreased expression of leukocyte integrins on their cell surface, decreased ability to aggregate in response to chemotactic stimuli, and decreased ability to migrate across bovine endothelial cell monolayers in vitro. Transendothelial migration of neutrophils from normal calves was reduced to levels comparable to the BLAD neutrophils by treatment with an anti-CD18 monoclonal antibody (MAb 60.3). Peripheral-blood lymphocytes from the BLAD calf also expressed negligible levels of leukocyte integrins, similar to their neutrophil counterparts. Our experimental findings in vitro correlate well with the clinical observations of decreased leukocyte trafficking and diminished host defense in leukocyte adhesion-deficient animals. The syndrome of BLAD may be a suitable model for one of the human leukocyte adhesion deficiency disorders.
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Leukocyte adhesion deficiency
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rIL-1 beta treatment of cultured human endothelial cells (HEC) promotes polymorphonuclear leukocyte (PMN) adhesion and transmigration. Using in vitro quantitative monolayer adhesion and videomicroscopic transmigration assays, we have examined the contributions of endothelial-leukocyte adhesion molecule-1 (ELAM-1), intercellular adhesion molecule-1 (ICAM-1), and the leukocyte adhesion complex, CD11/CD18, to these processes. Maximal enhancement of PMN adhesion and transmigration were observed after 4 h of rIL-1 beta treatment, when surface expression of ELAM-1 had peaked and ICAM-1 was modestly increased. Blocking mAb directed to either ELAM-1 or ICAM-1 inhibited greater than 90% of the up-regulated PMN transmigration. Blocking mAb directed to either CD11a/CD18 (LFA-1, a ICAM-1 counter-receptor), CD11b/CD18 (Mo-1), or CD18 (common beta 2-integrin) also blocked greater than 90% of PMN transmigration. At later time points (24 or 48 h), ELAM-1 surface expression was markedly decreased, whereas ICAM-1 expression was increased over the 4-h level; PMN adhesion remained elevated (approximately 50 to 60% of 4 h level), but transmigration returned to levels seen with unactivated HEC. These data indicate that PMN interaction with at least two distinct HEC adhesion molecules is necessary for transendothelial migration and suggests that PMN adhesion and transmigration, although interrelated, are mechanistically distinct processes.
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Intercellular adhesion molecule
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Objective To investigate the effect of changes in CD11/CD18 expressions on polymorphonuclear neutrophils (PMNs) in response to subeschar tissue fluid (STF) obtained from burn patients. Methods The expression of CD11a/CD18 on the membrane of STF-treated PMN from normal subjects and CD11b/CD18 were determined by flow cytometry, and the activity of myeloperoxidase (MPO) in the media was determined. Results In response to STF stimulation, the expression of CD11a/CD18 and CD11b/CD18 on the membrane of PMN increased, reaching its peak at 1 h, and maintained during the following 24 h. The activity of MPO in the media underwent almost the same process. Conclusion STF can activate the PMNs and stimulate the expression of CD11/CD18 on the membrane of PMNs.
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Objective:To observe the expression changes of adhesion molecules in peripheral blood leukocytes and serum soluble adhesion molecules in acute ischemic stroke after treatment with bartroxobin. Methods:Treatment group( n =8) was given bartroxobin (20 BU in 3 d) and other routine treatment;Control group( n =18) was similar to treatment group except for bartroxobin.The expression of CD11b,CD18,CD62L,CD54 on polymorphonuclear and monocyte were measured by flow cytometry, soluble ICAM 1 and VCAM 1 were measured by enzyme linked immunosorbent assay in consecutive patients[within 12,24,48 h( P 0.05) after stroke onset]. Results:Compared with control group, the mean fluorescence intensity of CD11b on polymorphonuclear decreased significantly in bartroxobin treatment group 48 h after stroke onset.No significant changes of CD11b expression on monocyte,CD18,CD62L,CD54 expression on polymorphonuclear and monocyte, serum level of soluble ICAM 1,VCAM 1 were detected. Conclusion:Decreasing adhesion molecule expression may not involve in the chief mechanism of bartroxobin in treatment of acute stroke.
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The role of the CD18 complex of leukocyte glycoproteins in adhesion-dependent functions of human leukocytes in vitro has been well documented. A ligand, intercellular adhesion molecule-1 (ICAM-1), for at least one member of the CD18 complex has been identified. This molecule is inducible on many cell types including vascular endothelium and keratinocytes by inflammatory mediators such as IL-1, TNF, and IFN-gamma. ICAM-1 has been shown to mediate, in part, the in vitro adhesion of lymphocytes and neutrophils to endothelial cells expressing ICAM-1. In the present study we have shown that mAb's to the human CD18 complex and to human ICAM-1 cross react with rabbit cells and that both anti-CD18 and anti-CD11b but neither anti-CD11a nor anti-ICAM-1 mAb's inhibit neutrophil migration, an adhesion-dependent function, in vitro. Pretreatment of rabbits with anti-CD18 and anti-ICAM-1 but not anti-CD11a mAb inhibited by greater than 60% neutrophil migration into PMA-induced inflamed rabbit lungs. This effect of anti-ICAM-1 mAb on pulmonary neutrophil influx after PMA injection has important implications. Specifically, that ICAM-1 can function as a ligand for CD18 and can mediate, at least in part, the migration of neutrophils to inflammatory sites.
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Cell–cell interaction
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The expression of several adhesion molecules is increased on the hepatic sinusoidal endothelial cells (SECs) in various liver diseases. The objective of this study is to assess the roles of intercellular adhesion molecule 1 (ICAM-1) and of CD18 in the interaction between the neutrophils (polymorphonuclear leukocytes [PMNs]) and SECs and in the injury to SECs mediated by PMNs. Rat PMNs was perfused on SECs stimulated with tumor necrosis factor alpha (TNF-alpha) using an in vitro flow system. The number of adhered PMNs to SECs and that of PMNs migrated under SECs was counted and the effects of anti-ICAM-1, anti-CD18, and dexamethasone were studied. We also define the effect of these antibodies on the SEC injury mediated by PMNs stimulated with phorbol 12-myristate 13-acetate (PMA) or N-formyl-methionyl-leucyl-phenylalanine (fMLP). TNF-alpha significantly increased the adhesion of PMNs to SECs (322 +/- 26 cells/mm2) compared with controls (194 +/- 22 cells/mm2). Anti-ICAM-1 and anti-CD18 significantly inhibited the adhesion of PMNs (131 +/- 10 and 51 +/- 30 cells/mm2, respectively). These antibodies also decreased the migration rate of PMNs (6.0% and 7.9%, respectively) compared with controls (migration rate, 21.2%). The SEC injury induced by PMA- and fMLP-activated PMNs was prevented by anti-ICAM-1 and anti-CD18. The adhesion of PMNs induced by TNF-alpha was inhibited by the treatment with dexamethasone (160 +/- 20 cells/mm2) via a down-regulation of ICAM-1 expression on SECs. The interactions between ICAM-1 and CD18 appeared to be important in the adhesion and the migration of PMNs to SECs. The injury to SECs was induced by the close interaction between the activated PMNs and SECs mediated via ICAM-1 and CD18.
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Activated leukocytes may be involved in the reperfusion injury of the brain. The expression of intracellular adhesion molecule-1 (ICAM-1) (CD54) and lymphocyte function-associated antigen-1 (LFA-1) (CD11a/CD18) are important for the interaction of activated leukocytes with the brain. Therefore, the expression of ICAM-1 in the cerebral vessels and LFA-1 on leukocytes were examined after reperfusion in a rat four-vessel occlusion model. Model rats underwent reperfusion (15, 30, and 60 min, and 6, 12, and 24 hrs) following 30 minutes of forebrain ischemia. Immunohistological staining for ICAM-1 and LFA-1 was performed in each subgroup. ICAM-1 expression increased after 1-hour reperfusion and persisted on the cerebral microvessels in both the subcortical region and the basal ganglia. Leukocytes stained by LFA-1 were observed in the capillary vessels after 6-hour reperfusion. Increased expression of ICAM-1 and LFA-1 were induced by reperfusion, and this may be important in reperfusion injury of the brain.
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Forebrain
Intercellular adhesion molecule
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Intercellular adhesion molecule
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Vascular permeability
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Abstract The β 2 ‐intergrin CD11a/CD18 binds to the intercellular adhesion molecules (ICAM)‐1 (CD54) and ICAM‐2. ICAM‐1 has a wide distribution, and its expression is up‐regulated by various cytokines. In contrast, ICAM‐2 has a more restricted distribution, and is mainly expressed on endothelial cells. In the present study we show that it is not induced by inflammatory cytokines or other treatments on any of several cells studied. Moreover, antibodies to the intercellular adhesion ligands were not able to block all CD11a/CD18‐dependent adhesion, indicating the presence of additional CD11a/CD18 ligands.
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Intercellular adhesion molecule
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