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  • 1
    Electronic Resource
    Electronic Resource
    Postoperative ulnar neuropathy after kidney transplantation (1984)
    Oxford, UK : Blackwell Publishing Ltd
    Anaesthesia 39 (1984), S. 0 
    Details
    ISSN: 1365-2044
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Postoperative ulnar neuropathy as a result of mechanical trauma at the elbow was observed in eight patients undergoing renal transplantation. In five cases this occurred on arms that were adducted during the operation and in which an arteriovenous shunt was present. In four cases (one patient had the lesion bilaterally) the other, abducted arm was affected. Analysis of possible causes revealed no single factor responsible for the condition. Factors that most likely contributed were: pressure on the adducted arm by the combined weights of patient and surgeon, blood pressure monitoring with a cuff compressing the cubital fossa, venous congestion by the arteriovenous shunt, and subclinical uraemic polyneuropathy. Although no single factor could be identified protection of the adducted arms with a hard plastic cover and placement of the blood pressure cuff as proximally as possible on the abducted arms provided a successful solution to the problem.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2044.1984.tb08935.x
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  • 2
    Electronic Resource
    Electronic Resource
    Endothelial Cells Promote Anti-CD3-Induced T-cell Proliferation via Cell-Cell Contact Mediated by LFA-1 and CD2 (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 38 (1993), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: T-cell activation requires not only T-cell receptor (TCR) engagement and subsequent TCR/CD3 cross-linking, but also one or more secondary activation signals generated by accessory cells (AC). We investigated the accessory function endothelial cells (EC) in an in vitro model for T-cell activation where the first cross-linking signal was delivered to peripheral human T lymphocytes by cither immobilized anti-CD3 monoclonal antibody (MoAb) or by PHA. In a previous report, we showed that EC provided a potent costimulatory signal in this model system. We have now analysed the nature of the EC-derived costirnulatory signal by testing whether EC could be substituted by cy lokines. by studying the effect of EC fixation and by testing the involvement of a number of adhesion molecules. Our findings indicate that EC accessory function is mediated mainly by membrane-bound factors. The nature of these membrane-bound factors was analysed by studying the inhibitory properties of a series of MoAbs directed against several adhesion molecules. Antibodies directed against CD44, E-selectin, CD31, CD26, B7/BBI, VLA-4 or VCAM-1 were not inhibitory. However, an inhibition, was clearly observed with antibodies against LFA-1 and CD2. Remarkably, this inhibition was not found with MoAbs to their respective counterstructures ICAM-1 and LFA-3. In summary, we postulate that both LFA-l/ICAM-1, and CD2 LFA-3 interactions are involved in EC accessory function, although the role of the EC-associated adhesion partners is not fully understood.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1993.tb02585.x
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  • 3
    Electronic Resource
    Electronic Resource
    The Human Fc Receptor for Mouse IgG2b on Monocytes and EBV-B Cells is Functionally Inhibited by Anti-HLA Class II Antibodies (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 37 (1993), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have recently described a polymorphic Fc receptor for murine IgG2b (mIgG2b), present on human monocytes and EBV-transformed B lymphocytes. The present study shows that anti-HLA class II monoclonal antibody (MoAb) completely inhibits both the (Fc receptor-dependent) T-cell proliferation, induced by mIgG2b anti-CD3 MoAb, and rosetting with mIgG2b-sensitized erythrocytes. This inhibition is also observed with F(ab′)2 fragments of anti-HLA class II MoAb, and is therefore not Fc mediated. The Fc receptor for mIgG2b is also present on EBV-transformed B cells obtained from a patient with‘bare lymphocyte syndrome′, that completely lack HLA class II antigens. Therefore, the Fc receptor for mIgG2b and HLA class II antigens are not identical. Since the low affinity receptor for IgE (FcɛII; CD23) was reported to be associated at the cell surface with HLA class II antigens, we have compared both types of Fc receptor, and observed that human IgE strongly inhibits the mitogenic effect of murine IgE anti-CD3 but not of mIgG2b anti-CD3 MoAb. We conclude that the human Fc receptor for mIgG2b is strongly inhibited by anti-HLA class II MoAb, but is not identical to HLA class II or FcɛRII.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1993.tb01756.x
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  • 4
    Electronic Resource
    Electronic Resource
    Analysis at the DNA Level of Human FcγRII Isoforms in Relation to the Polymorphic Binding of Murine IgG2b to Human B Cells (1996)
    Oxford, U.K. and Cambridge, USA : Blackwell Science Ltd
    Scandinavian journal of immunology 44 (1996), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Three classes of human leucocyte Fcγ receptors (hFcγR) have been identified so far: hFcγRI, hFcγRII, and hFcγRIII. Previous studies have demonstrated that genetically determined differences between individuals exist both with respect to the binding of murine IgG1 (mIgG1) to hFcγ receptors, and with respect to the binding of murine IgG2b (mIgG2b). The polymorphism in binding of mIgG1 could be ascribed to hFcγRIIA, an isoform of hFcγRII. The authors have now investigated whether one of the isoforms of hFcγRII is also responsible for the polymorphism in binding of mIgG2b. In these studies the authors used EBV-transformed human B cells that demonstrated either binding or no binding of mIgG2b in EA-rosetting assays. mRNA obtained from these cells was amplified by reverse transcriptase and polymerase chain reaction (RT-PCR). Hybridization experiments with the RT-PCR products revealed that the hFcγRIIB but not the hFcγRIIA isoform was present in these cells. DNA sequencing further demonstrated that the nucleotide sequence of both the extracellular part and the cytoplasmic moiety of hFcγRIIB was identical for all individuals tested, regardless of their ability to bind mIgG2b. These findings indicate that the polymorphic binding of mIgG2b cannot be ascribed to one of the isoforms of hFcγRII. Since hFcγRI and hFcγRIII are not present on the cell surface of these cells, the authors conclude that an Fc receptor different from the known hFcγ receptors must be responsible for the polymorphic binding of mIgG2b. These data further expand the complexity of hFcγR.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-3083.1996.d01-348.x
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  • 5
    Electronic Resource
    Electronic Resource
    Proteolysis Increases the Fc-Mediated Binding of Murine IgG2b to Human EBV-Transformed B Cells, but Decreases the Expression of FcγRII and FcγRII (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 38 (1993), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have previously described a polymorphic human Fc receptor for murine IgG2b (mIgG2b). This receptor was defined by the binding of (complexed) mIgG2b to monocyles and Epstein-Barr virus (EBV)-transformed B cells. Three per cent of normal individuals were high responders with respect to mIgG2b (mIgG2b-HR), whereas the other individuals were low responders for mIgG2b (mlgG2b-LR). In the present study we investigated the effect of proteolytic enzymes on the Fc-mediated binding of mIgG2b to EBV-B cells. Pronase, human leucocyte elastase and cathepsin G caused an inereased binding (in an EA-rosetting assay) of mIgG2b to EBV-B cells from mIgG2b-HR, but not from mIgG2b-LR. Simultaneous immunofluorescence studies demonstrated that these protcolytic enzymes strongly reduced the expression of FcγRII and FcγRII on these cells, whereas HLA class I or HLA class II molecules were not affected. These findings strongly suggest that binding of mIgG2b is not mediated by FcγRII or FcγRII We also studied the effect of proteolysis on mIgG2b-HR EBV-B cells from an HLA class II-negative individual. In this case EA-mIgG2b rosetting was decreased after proteolysis, suggesting that HLA class II molecules may have a role in protecting the binding site for mIgG2b against proteolytic destruction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1993.tb01723.x
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  • 6
    Electronic Resource
    Electronic Resource
    Accessory Function of Endothelial Cells in Anti-CD3-Induced T-Cell Proliferation: Synergism with Monocytes (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 35 (1992), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Monoclonal antibodies to CD3 can induce proliferation of resting T cells. In vitro this effect is dependent on the presence of monocytes. They serve as accessory cells providing a co-stimulatory signal after cross-linking of the antibody-coated TcR/CD3 complex by the Fc receptor on the monocytes. We have studied whether endothelial cells can replace monocytes with regard to (his function. Highly purified T-cell preparations were cultured in the presence of anti-CD3 antibody, purified monocytes, and human umbilical vein endothelial cells. Anti-CD3 and endothelial cells alone were unable in support T -cell proliferation, due to lack of FcR expression. Addition, however, of as few as 10110 FcR+ monocytes (0.8% of the number of T cells present) to a co-culture of T cells and endothelial cells (EC) in the presence of soluble anti-CD3 resulted in a strong proliferation of T cells. When anti-CD3 was presented in an immobilized form (coated to the culture well or to Sepharose beads), or when phytohaemagglutinin was added to the culture as a cross-linking agent, EC could support T-cell proliferation in the absence of any monocytes. We conclude that EC by themselves cannot support the proliferation of pure T cells induced by soluble anti-CD3, but are potent generators of the co-stimulatory signal(s). They provide a suitable starling material to further define this co-stimulatory activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1992.tb02880.x
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  • 7
    Electronic Resource
    Electronic Resource
    Characterization of Two Fc Receptors for Mouse Immunoglobulins on Human Monocytes and Cell Lines (1987)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 26 (1987), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have previously reported a polymorphism in the mitogenic effect of murine (m) IgG1 anti-CD3 monoclonal antibodies. This polymorphism was genetically determined and could be attributed to polymorphism of the Fc receptor (FcR) for mIgG1 present on human monocytes. We have now extended these studies by quantitating FcR expression on monocytes and cell lines by a recently developed EA rosette assay, using the erythrocyte-associated pseudoperoxidase activity. The data show that the polymorphism of the monocyte FcR for mIgG1 is based on a quantitative rather than an absolute difference. Furthermore, this FcR is specific for mIgG1 and does not bind mIgG2a or mIgG2b nor, surprisingly, human IgG. The expression of this FcR on cell lines correlates with their accessory function in IgG1 anti-CD3-induced T cell proliferation. mIgG2a can inhibit the rosetting of monocytes with erythrocytes sensitized with human IgG. The FcR detected by this rosette technique can interact with all four human IgG subclasses but not with mIgG1 or mIgG2b. The expression of this type of FcR on human cell lines correlates well with their ability to support mIgG2a anti-CD3-induced mitogenesis. These direct measurements of FcR expression support the concept that human monocytes have two independent FcR with affinity for mouse IgG: one receptor specigic for mIgG2a (which also binds human IgG), and a second specific for mIgG1.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1987.tb02302.x
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  • 8
    Electronic Resource
    Electronic Resource
    Cytomegalovirus infection and disease in renal transplant patients treated with cyclosporin (1989)
    Springer
    Transplant international 2 (1989), S. 92-95 
    Details
    ISSN: 1432-2277
    Keywords: Cytomegalovirus infection in kidney transplantation ; Cytomegalovirus disease and rejection ; Rejection and cytomegalovirus disease ; Risk factors for cytomegalovirus disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In this prospective study, the incidence of cytomegalovirus (CMV) infection and CMV disease was determined in 175 renal transplant recipients on cyclosporin and low-dose prednisone. CMV infection occurred in 51.4% of the patients, CMV disease in 13.7%. The major manifestations of CMV disease were fever of unknown origin and leukopenia. In the group with CMV infection, there was an increased occurrence of rejection (60% in infected vs 27% in noninfected patients). In most patients (41/54), the rejection preceded the CMV infection. CMV infection did not lead to a decreased graft survival. There was no close time relationship between the onset of clinical symptoms of CMV disease and the laboratory confirmation of CMV infection. A subgroup of patients at risk for the development of severe CMV disease could not be identified.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02459326
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  • 9
    Electronic Resource
    Electronic Resource
    Renal allograft artery stenosis: results of medical treatment and intervention. A retrospective analysis (1993)
    Springer
    Transplant international 6 (1993), S. 111-115 
    Details
    ISSN: 1432-2277
    Keywords: Renal artery stenosis ; Hypertension, renal artery stenosis ; Percutaneous angioplasty, renal artery stenosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In a retrospective analysis of 1165 renal transplantations in our center, 65 cases of renal allograft artery stenosis were diagnosed angiographically (prevalence 5.5%). Hypertension was present in all case; a bruit over the allograft and an increase in serum creatinine level were additional reasons for angiography. Shortly after diagnosis of the stenosis, two patients died and two others lost their grafts due to thrombosis. In 24 patients the decision was made not to correct the stenosis. One of these grafts was lost because the stenosis could not be corrected. Medical management of hypertension in these patients resulted in a decrease in diastolic blood pressure from 109±22 to 96±12 mm Hg (P〈0.01) 3 months after diagnosis with the use of almost twice as many antihypertensive drugs as at the time of diagnosis (P〈0.01). The stenosis was corrected if the angiography showed it to be so severe that it jeopardized renal allograft function or caused uncontrollable hypertension. Only three of nine percutaneous transluminal angioplasty (PTA) procedures resulted in a definitive correction of the stenosis. Surgical intervention was performed in 30 patients, including two patients whose PTAs had proved unsuccessful. Surgery led to graft loss due to thrombosis in 6 of 30 operations (20%), whereas restenosis occurred twice (7%). In three other case (10%), the correction was not successful due to local anatomical variations or concomitant rejection. Successful correction of the stenosis by either PTA or surgical intervention (n=22) resulted in a significant decrease in systolic (171±31 vs 145±27 mm Hg; P〈0.01) and diastolic (103±15 vs 89±14 mm Hg; P〈0.05) blood pressures 3 months after correction. Concomitantly, a decrease in the number of antihypertensive drugs from 2.1±1.0 to 1.5±1.0 (P〈0.01) was achieved. In conclusion, renal allograft artery stenosis could successfully be managed pharmacologically, provided that allograft perfusion was not jeopardized. Successful surgical correction of a stenosis with effective control of hypertension was achieved in 63% of the cases. PTA was less frequently successful but did not cause any graft loss.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00336655
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  • 10
    Electronic Resource
    Electronic Resource
    Principles of immunosuppression and rejection therapy (1988)
    Springer
    World journal of urology 6 (1988), S. 112-115 
    Details
    ISSN: 1433-8726
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The continuous exposure of the graft to the immune system of the host makes lifelong immunosuppressive treatment after renal transplantation necessary. In the basic immunosuppressive treatment regimes, azathioprine has largely been replaced by the much more potent ciclosporine. The major drawback of ciclosporine is its nephrotocicity. Results of controlled trials have demonstrated that this problem can be circumvented by conversion from ciclosporine to azathioprine treatment at 3 months posttransplantation. Prednisone given orally in low doses has retained its place as a useful adjunct to the basic regimes. Acute rejection episodes can be treated with large IV doses of prednisolone, high-dose oral prednisone, or anti-T-cell antibodies. The latter approach is the most effective. Both polyclonal and monoclonal anti-T-cell antibodies have been used, but a controlled comparison of their efficacy has not been made. The preparation of agents that interfere with the interleukin-2 receptor on activated T cells represents an exciting new development. These agents could theoretically eliminate T cells triggered in the immune response against the graft, leaving resting T cells unharmed. These new approaches hold promise for future improvements of immunosupressive treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00326625
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