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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 36 (1992), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Several studies during recent years have demonstraled the potential for vascular smooth musele cells (SMC) and dermal fibroblasts to participate in immune interactions such as antigen presentation and allorcactivity. The molecular interactions mediating lymphocyte adhesion to these mesenchymal cells have, however, not previously been eharacterized in detail. In the present study we demonstrate ICAM-1 (CD54) expression by cultured human SMC and its up-regulation by IL-1. IFN-γ, and bacterial lipopolysaccharide. Monoclonal antibodies were used to define ihe molecular interactions in the adhesion of 51Cr-labelled T lymphoblasts to adherent SMC and fibroblasts. ICAM-1 appeared lo mediate adhesion ofT lymphocytes by binding to the β2 integrin CDlIa/CD18 (LFA-1) expressed by ihe lymphoblasts. We present evidence for the involvement of at least three different mechanisms in ihe adhesion of activated T lymphocytes to cultured fibroblasts. It was found that β2-integrin-mediated interaction could only account for less than half of the binding activity. The remaining adhesion was partly mediated by β2-integrins, presumably via VLA-5 since an anti-VLA-5 antibody and an RGD-containing peptide blocked adhesion to the same degree. However, antibodies to β1-, β2, and β3-integrin subunits added together only inhibited adhesion by approximately 50% The residual adhesion could be blocked by inhibition of cell metabolism an d was increased by stimulation of the lymphocytes with phorbol ester, suggesting involvement of other, as yet undefined, adhesion molecules. The molecular interactions between lymphocytes and mesenchymal cells demonstraled in this study may have implicalions in several inflammatory conditions such as vaseulitis, atherosclerosis, and connective tissue diseases.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK; Malden , USA : Blackwell Science Ltd
    Scandinavian journal of immunology 59 (2004), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Severe hypercholesterolaemia is associated with decreased levels of immunoglobulin G2a (IgG2a) antibodies [T-helper 1 (Th1) response] to modified malondialdehyde-modified low-density lipoprotein (MDA-LDL) and increased levels of Th2-dependent IgG1 antibodies in apolipoprotein E-deficient (apoE–/–) mice. To investigate whether this reflects a general pattern of metabolic regulation of the humoral immune response, apoE–/– mice were fed diets resulting in different degrees of hypercholesterolaemia and immunized with keyhole limpet haemocyanin (KLH) in aluminium hydroxide. Cholesterol levels for different treatment groups ranged from 14 to 77 mmol/l in serum and from 10 to 39 mmol/g in liver. Mice with severe hypercholesterolaemia had increased IgG1 antibodies to MDA-LDL and decreased IgG2a anti-MDA-LDL. Importantly, titres of IgG2a antibodies to KLH were also decreased, while IgE anti-KLH was increased, with a corresponding induction of interleukin-4 (IL-4) and IL-10 and a decrease in interferon-γ (IFN-γ) in KLH-stimulated spleen cells in vitro. Thus, hypercholesterolaemia clearly affects antibody production both to the autoantigen MDA-LDL and to the exogenous antigen KLH, favouring antibody isotypes (IgG1 and IgE) that are dependent on Th2 help to B cells. Nuclear receptors ligated by oxidized lipid derivatives modulate T-cell responses, and it is speculated that this mechanism may cause the switch to Th2 in severe hypercholesterolaemia.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Dendritic cells (DCs) have been identified as effective antigen-presenting cells (APCs). We demonstrate that extracellular matrix (ECM), hyaluronic acid (HA) and chondroitin sulphate A (CSA), in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF), can rapidly promote the differentiation of monocyte-derived immature DCs, as characterized by the remarkable upregulation of human leucocyte antigen (HLA-DR), CD40, CD54, CD80 and CD86 expression to levels higher than those in the DCs generated by culturing with GM-CSF and interleukin (IL)-4 for 7 days and aggregation of the cells within 48 h. The upregulation of expression of HLA-DR, CD40, CD54, CD80 and CD86 was dose-dependent. Further studies showed that HA and CSA were able to augment nuclear factor (NF)-κB activity, as determined by gel mobility shift assay and promote protein phosphorylation. Inhibition of NF-κB by pyrolidine dithiocarbamate and sodium salicylate, and serine-threonine and tyrosine kinase by starosporine as well as phosphatidylinositide-3-kinase (PI-3-K) by wortmannin could prevent the effects of HA and CSA on the expression of HLA-DR, CD40, CD80 and CD86 in various degrees. Thus, our data demonstrate that HA or CSA can effectively and rapidly promote the differentiation of immature DC, suggesting that HA and CSA may possess a potential capacity in regulating immune responses.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 42 (1995), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The macrophage scavenger receptor (MSR) is a multipotent receptor that mediates uptake of macromolecules with clustered negative charges, such as endotoxins and oxidized proteins and lipoproteins. It may also serve as an adhesion molecule for monocytes and macrophages. We have analysed MSR expression in human peripheral lymph nodes and show, by reverse transcription-PCR, that the type I isoform of MSR is abundantly expressed in this tissue. With the use of a new set of isoform-specific peptide antibodies, both isoforms of MSR were detected in the cuboidal endothelium of high-endothelial venules (HEV). MSR antibodies also stained macrophages and follicular dendritic cells of germinal centres. These data indicate that the MSR gene is expressed in HEV endothelium in vivo. It is suggested that MSR expression may be important for antigen uptake and leucocyte adhesion to HEV in the lymph node.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Allergy 50 (1995), S. 0 
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have studied the induction of nitric oxide during late allergic responses, using a guinea pig model of trimellitic anhydride (TMA)-induced airway allergy. TMA is a low molecular weight chemical which can cause occupational asthma. The activity of nitric oxide synthase (NOS) was investigated by the detection of 3H-labeled citrulline formation from 3H-labeled arginine. In sensitized animals, challenge with TMA conjugated to guinea pig albumin (TMA-GPSA) increased the activity of Ca2+ -independent NOS (inducible NOS; iNOS) in lung and bronchial tissues at 15–17 h after challenge compared to nonsensitized animals. The induction of iNOS activity was associated with an increased level of nitrite, an end metabolite of the 1-arginine-NO pathway, in bronchoalveolar lavage fluid. In contrast to iNOS, the activity of Ca2+-dependent NOS (constitutive NOS; eNOS) was not affected by the allergen challenge. These results demonstrate that iNOS in bronchial tissue is induced late after allergen challenge in sensitized guinea pig.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-198X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1437-160X
    Keywords: Rheumatoid arthritis ; Osteoarthritis ; Complement system
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The decay-accelerating factor (DAF) is a complement regulatory cell surface protein that protects cells from complement-mediated lysis. We analysed synovial tissue biopsies from patients with chronic arthritides for the presence of DAF using immunohistochemistry. DAF was expressed in the synovial lining cell layer both in rheumatoid arthritis (RA) and in osteoarthritis (OA). DAF was also on vascular endothelial cells of synovial tissue. A significant correlation was found between the expression of DAF and of HLA-DR in the lining layer, suggesting that DAF may be induced during a local inflammatory response. In addition, C5b-9 terminal complement complexes were found in several DAF-positive cases, suggesting that complement activation might, in itself, induce DAF expression. We propose that the occurrence of DAF may represent a physiological mechanism for local complement regulation in synovial tissue.
    Type of Medium: Electronic Resource
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