Virus receptors and cell tropisms.
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Animals↗
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Complement activation and CD59 expression in the motor facial nucleus following intracranial transection of the facial nerve in the adult rat.
Intracranial transection of the facial nerve has been shown to cause a massive neuronal cell death in the motor facial nucleus. Complement activation has been proposed to contribute to neuronal degeneration following axotomy. Using immunocytochemistry and in situ hybridization we show in the present study that there is complement activation in the facial nucleus after intracranial facial nerve transection as well as increase of the complement regulators CD59 and clusterin. We propose a neuroprotective role for the complement regulators CD59 and clusterin against homologous attack of complement to facial motor neurons.
Age Factors↗
A clinical and virological study of hepatitis C virus-related cryoglobulinemia in Germany.
BACKGROUND/AIMS: Several reports, especially from Southern Europe, have demonstrated a close association between hepatitis C virus (HCV) infection and mixed cryoglobulinemia. In this study we have analyzed the significance of HCV-related cryoglobulinemia in Germany. METHODS: Sera from 79 patients with cryoglobulinemia of type I (n=21), II (n=28) or III (n=30) were investigated for HCV markers. Furthermore, 132 consecutive patients with chronic hepatitis C were studied for the presence of cryoglobulins. Genotypes of HCV were determined according to Simmonds, and HCV-RNA concentrations were measured in patients with and without cryoglobulinemia. RESULTS: In 79 patients with cryoglobulinemia we found anti-HCV antibodies in 17 (22%) and HCV-RNA in 11 patients (14%). HCV antibodies were more frequent in essential (44%) compared to secondary mixed cryoglobulinemia (15%). In 132 patients with chronic HCV infection cryoglobulins were detected in 37 patients (28%), in 21 of them at low levels. Clinical symptoms due to cryoglobulinemia were observed in eight of the 37 patients, severe vasculitis in three patients with high cryocrit-levels and cryoprecipitation at room temperature. HCV genotype 1 and subtype 1b were most prevalent, both in patients with and without cryoglobulinemia, and mean HCV-RNA levels were not different between the two groups. Comparison of HCV-RNA levels in cryoprecipitates, supernatant and native serum suggests binding of HCV-RNA to the cryoprecipitate with different affinity in individual patients. CONCLUSIONS: The lower prevalence of HCV-related cryoglobulinemia in our study compared with data from Italy and France suggests a south-north gradient in the prevalence of HCV-associated cryoglobulinemia in Europe.
Adult↗
Acute phase haemolysis in chronic cold agglutinin disease.
We previously described a paradoxical form of chronic cold agglutinin disease (CAD) in which haemolysis occurred during episodes of fever but only marginally during exposure to colds. In order to investigate the molecular basis for this response we performed a 12-month prospective study of a patient with CAD and paradoxical haemolysis. Blood samples were collected monthly during health, and daily following hospitalization owing to hip fracture. During health we observed decreased levels of C3, undetectable C4, a non-functional classical pathway and a normal alternative pathway. Increased concentrations of C1-INH/C1rs complexes indicated continuous formation of C1-antibody-antigen complexes. There was a low-grade temperature-dependent fluctuating haemolysis as evidenced from measurements of lactate dehydrogenase. Following the hip fracture, the haemolysis increased. Levels of interleukin (IL)-1beta, IL-6, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha increased as did C1-INH, C3, C4, CRP, and lactate dehydrogenase. The results support our hypothesis stating that paradoxical haemolysis in CAD is controlled by the availability of early classical pathway complement molecules and that haemolysis following acute phase responses occurs as a consequence of increased complement synthesis.
Acute Disease↗
Effect of circulating immune complexes on transfusional therapy in patients with hemophilia or von Willebrand's disease.
Circulating immune complexes were examined in patients with hemophilia or von Willebrand's disease in order to determine the immediate or long-term side effects after transfusion. The conglutinin binding assay which allows quantitation of C3bi-bearing immune complexes was used for 82 patients with hemophilia A. Immune complexes were detected in 37 (45%) of these cases prior to transfusion. Immune complexes also were detected in four of 11 patients with hemophilia A and factor VIII inhibitors, in five of 11 patients with hemophilia B, and in three of 10 patients with von Willebrand's disease. The levels of circulating immune complexes in 21 patients with hemophilia A and seven with von Willebrand's disease significantly increased 24 hours after concentrate or cryoprecipitate transfusions. Purified immune complexes from three patients with hemophilia A were shown to contain IgG, IgM, and complement components. No factor VIII coagulant or antigenic protein or fibrinogen was identified in the immune complexes using specific antisera. Side effects immediately after transfusion were not associated with immune complexes. The levels of factor VIII or IX after transfusion were not particularly decreased in relation to the presence of immune complexes. Finally, the presence of circulating immune complexes in the patients studied did not correlate with the number of transfusions, the units of concentrates injected, the presence of HBsAg or HbsAb, the levels of plasma aspartate transferase, or the presence of rheumatoid factor. Proteinuria was absent in all the patients studied.
Antigen-Antibody Complex↗
'Immune complex' mediated intravascular hemolysis due to IgM cephalosporin-dependent antibody.
Immune hemolytic anemia (IHA) related to cephalosporins is rare and generally considered to be the result of a drug-adsorption mechanism. In previously reported cases, the hemolysis was usually extravascular and the causative antibodies were IgG, incapable of activating complement, and demonstrable by the direct or indirect antiglobulin test using red cells (RBCs) pretreated in vitro with cephalosporin. The authors report a patient in whom acute intravascular hemolysis developed while she was receiving cefotaxime (a cephalosporin as yet not reported to cause IHA). The patient's RBCs were coated only with complement fragments (C3d), even at the peak of the hemolytic episode. Her serum and eluates repeatedly yielded negative results when tested against normal or cephalosporin-coated RBCs. However, strong hemagglutination and C5b-9-mediated hemolysis were observed if the patient's serum was tested against RBCs in the presence of the drug, its ex vivo antigen and, to a lesser degree, cephalothin and ceftriaxon, but not in the presence of penicillin and other related cephalosporins. The positive reactions were not changed by preincubating the serum with different amounts of the drugs. All of these findings reflect the typical picture of drug-induced IHA by the so-called "immune complex" mechanism and not by the drug-adsorption mechanism. The authors conclude that cephalosporin can cause immune hemolysis in two ways: the drug-adsorption mechanism and, as described here, the "immune complex" mechanism.
Aged↗
Helicobacter pylori urease significantly reduces opsonization by human complement.
The role of Helicobacter pylori urease in opsonization by human complement was investigated. H. pylori wild type strain N6 and isogenic mutants lacking either the large urease subunit (UreB) or an accessory urease protein (UreG) were incubated with different sera. C3b bound to the bacteria was measured by specific staining and flow cytometry. As compared with opsonization of N6 and the UreG-lacking mutant, opsonization of the UreB-lacking mutant was significantly increased after incubation with sera from both H. pylori uninfected (P<.001) or infected (P<.05) persons. However, when sera from uninfected persons were used, effective opsonization of this mutant proved to be dependent mainly on the classical pathway of complement activation. Irrespective of the serum used, opsonization values were very low after selective inactivation of the classical or the alternative pathway. Reduced opsonization of the urease-expressing strains could, to some extent, result from degradation of bound C3b.
Bacterial Proteins↗
A sialic-acid-specific lectin from Cepaea hortensis that promotes phagocytosis of a group-B, type-Ia, streptococcal strain.
Group-B streptococci that possess a type-specific surface polysaccharide undergo phagocytosis only in the presence of antibodies to this, and complement. The snail Cepaea hortensis forms a lectin that is specific for sialic acid; treatment with this promoted the phagocytosis of a group-B streptococcus of serotype Ia (strain O90) in the absence of opsonic antibodies. The effect of the lectin was dose-dependent and required the presence of complement. The specificity of the lectin reaction for sialic acid was proved by the inhibition of phagocytosis by bovine submaxillary mucin. The participation of complement in the reaction was confirmed by demonstrating that C3 was bound to the surface of lectin-treated cells.
Animals↗
The use of SnB to determine an anomalous scattering substructure.
The positions of eight Se atoms in a selenomethionyl 35 kDa protein were determined at 2.0 and 2.5 A resolution using the direct-methods program SnB. Data at the selenium peak, edge and remote wavelengths were measured and processed independently. Anomalous difference E magnitudes at each wavelength were derived by two different procedures: renormalized diffE values were calculated according to the equation diffE = ¿sigma[(f + f')2 + f"2]||E+|-|E-||¿1/2/2q(sigma f"2)1/2, where q is a least-squares fitted renormalization function of sinstraight theta/lambda such that = 1.0; and difference E magnitudes were calculated from DeltaF2. Locally normalized E magnitudes corresponding to |FA| were also derived from the combination of the data at all three wavelengths through the use of the MADSYS program suite. Each of the independent sets of anomalous difference E magnitudes was capable of producing the correct solution, as did the E data obtained from the FA data. Higher success rates with SnB were observed for the 2.0 A peak and edge diffE data.
Complement C3d↗
Effects of 3-azidothymidine on platelet counts, indium-111-labelled platelet kinetics, and antiplatelet antibodies.
Treatment of the acquired immunodeficiency syndrome with 3-azidothymidine (zidovudine; AZT) can induce severe neutropenia and anemia, while platelet counts increase. In order to understand the mechanism by which this favorable effect on platelets is induced, we prospectively studied platelet kinetics and platelet serology in 8 hemophiliacs receiving the drug. All patients underwent a second investigation after 3 months of treatment. Four patients were thrombocytopenic before treatment. Platelet counts increased significantly already after 1 week of treatment (p = 0.03), when only 3 patients remained thrombocytopenic. In these latter patients a further increase of platelet counts was noticed during the following 3 months. Platelet life-span was shortened in all patients at the initial investigation and a significant prolongation was measurable at the second evaluation (p = 0.015). Platelet-associated immunoglobulin G was increased in 3 patients at the first investigation and in 4 patients at the follow-up. Platelet-associated complement (PAC3d) was elevated in all subjects at the first determination. It decreased in 6, but increased in 2 patients thereafter; thus these changes did not become significant (p = 0.078). Immunofluorescence studies revealed antiplatelet antibodies in 7 patients' sera before treatment, and in 5 sera during drug therapy. At both investigations, the antibodies bound to the platelet glycoprotein IIIa as was demonstrated by immunoprecipitation of radiolabeled platelet proteins. We conclude, that AZT treatment improves platelet counts in HIV-infected hemophiliacs primarily by a prolongation of platelet survival without having a significant influence on antiplatelet antibody binding.
Autoantibodies↗
CD8+ lymphocyte decrease in HIV disease: association with anti-CD4+ but not with anti-CD8+ lymphocyte autoantibodies.
HIV+ patients form autoantibodies against CD4+ and CD8+ lymphocytes. It was shown that anti-CD4+ lymphocyte autoantibodies are associated with the depletion of CD4+ cells. In the present study we analyzed the relationship of anti-CD4+ and anti-CD8+ autoantibodies with the CD8+ lymphocyte decrease commonly observed during HIV disease. IgM and IgG antibodies as well as complement fragments were determined on the surface of CD4+ and CD8+ lymphocytes using double fluorescence flow cytometry. Anti-CD8+ lymphocyte autoantibodies were found more often in HIV + hemophilia patients (75/105 = 71%) than HIV- hemophilia patients (13/37 = 35%; p < 0.0001), patients with pharyngeal carcinoma (20/44 = 45%; P = 0.002), habitual abortions (3/13 = 23%; p = 0.0009) or healthy individuals (93-223 = 42%; p < 0.0001). Anti-CD8+ antibodies, mostly of the IgM type, occurred significantly more frequently than anti-CD4+ antibodies in healthy controls (p < 0.0001), patients with pharyngeal carcinoma (p = 0.0001), or HIV- patients (p = 0.01). In HIV+ patients, however, anti-CD4+ autoantibodies were found more often than anti-CD8+ antibodies (85 vs 71%; p = 0.02). 70 of 104 (67%) HIV+ patients had autoantibodies on both CD4+ and CD8+ lymphocytes and the IgG/IgM/C3d autoantibody pattern was identical in 31 (44%) of the patients. Interestingly, peripheral blood CD8+ cell counts were significantly associated with anti-CD4+ (p = 0.01) but not with anti-CD8+ lymphocyte autoantibodies. It is hypothesized that the inhibition and depletion of CD4+ cells by anti-CD4+ autoantibodies is associated with a loss of regulatory functions that leads to a depletion of antiviral cytotoxic CD8+ lymphocytes.
Autoantibodies↗
Molecular modelling of human complement component C3 and its fragments by solution scattering.
Solution scattering experiments using both X-rays and neutrons are reported for human complement component C3 and up to six other glycoprotein fragments that are derived from C3. The X-ray and neutron molecular masses and neutron matchpoints are in agreement with the known primary sequence of C3. The X-ray radius of gyration RG of C3 is 5.2 nm and is similar for the related forms C3u, C3(a + b) and C3b. The X-ray cross-sectional radius of gyration RXS of C3b is however less than that of C3, C3u and C3(a + b). The major fragments of C3b, namely C3c and C3dg, were studied. The RG of C3c is 4.7 nm and for C3dg is 2.9 nm. C3c and C3dg do not interact when they coexist in solution in equimolar amounts. When C3u is cleaved into iC3u, the RG of iC3u increases to 5.9 nm and its RXS decreases, showing that C3c and C3dg behave as independent entities within the parent glycoprotein. Analyses of the neutron RG and RXS values by contrast variation techniques confirm the X-ray analyses, and show no evidence for significant hydrophobic or hydrophilic domains within C3 or any of its fragments. Shape analyses show that C3, C3c and C3dg are elongated particles. Debye models were developed using the scattering curve out to Q = 1.6 nm-1. These show that C3 and C3c resemble oblate ellipsoids while C3dg resembles a prolate ellipsoid. C3dg lies on the long edge of C3c within C3. The dimensions of the models are 18 nm X 2 nm X 10 nm for C3, 18 nm X 2 nm X 7 nm for C3c and 10 nm X 2 nm X 3 nm for C3dg. These models are compatible with analyses of the scattering curve RG and RXS values, data from sedimentation coefficients, and images of C3 and C3c seen by electron microscopy.
Complement C3↗
Heparin-coated equipment reduces complement activation during cardiopulmonary bypass in the pig.
Complement activation was studied during cardiopulmonary bypass (CPB) in the pig. One group of animals was perfused for 2 h using a standard extracorporeal circuit including a hollow fiber membrane oxygenator with full systemic heparinization. Another group was treated in the same way, except that bypass was performed through a heparin-coated CPB circuit (Carmeda Bio-Active Surface, CBAS) and systemic heparinization was reduced by 75%. It was found that complement activation during CPB, measured as changes in the ratio C3d/C3, was significantly less in the CBAS group, most probably reflecting a better biocompatibility.
Animals↗
Absence of brain antibodies in the sera of relapsing-remitting multiple sclerosis patients is not due to the formation of immune complexes.
Using an enzyme-linked immunoadsorbent assay, we looked, whether the formation of idiotype-anti-idiotype complexes was responsible for the absence of antibodies in the sera of MS patients. We tested 18 relapsing-remitting and 26 chronic progressive patients versus 44 age- and sex-matched controls. We did not find elevated titres of immune complexes in the sera of the multiple sclerosis patients.
Adult↗
The influence of polyethylene glycol precipitation and of ageing plasma and serum on the measurement of C3dg/d.
In plasma and serum samples, ageing results in excessive C3dg/d values when measured by electroimmunoassay. The use of polyethylene glycol, either in the preparation of the samples or in the electrophoretic gels, gives falsely low values.
Chemical Precipitation↗
Leukocytes, eosinophils and complement function during hemodialysis with polysulphone and polymethylmethacrylate membranes: comparison with cuprophan and polyacrylonitrile.
The biocompatibility of the two new dialysis membranes, polysulphone (PS) and polymethylmethacrylate (PMMA), was evaluated versus cuprophan (CUP) and polyacrylonitrile (PAN) by studying the in vivo effects of the four different membranes on leukocyte counts, eosinophil levels and complement function both in the presence and absence of dialysis fluid. Complement function was also examined in vitro by studying the generation of chemotactic factors, whole complement activity and C3d serum conversion. Passive absorption of complement fractions by membranes has completed in vitro studies. PS, PMMA and PAN showed a higher biocompatibility than CUP, even if slight differences can be observed: PS showed a PAN-like biocompatibility pattern with a relatively high absorption of complement factors by the membrane and without complement activation. On the other hand, PMMA showed a CUP-like pattern and caused complement activation, even though to a lower intensity than CUP. PMMA biocompatibility appears to stand in-between CUP and the other two synthetic membranes PS and PAN. Our results confirm the important role played by membrane-induced complement activation on hemodialysis leukopenia. Dialysis fluid does not have a significant influence on membrane biocompatibility, but represents the major factor in determining intradialytic eosinopenia. Eosinophils seem to represent a more important marker of dialysis than of membrane biocompatibility.
Acrylic Resins↗
Renal lesion of type Ia glycogen storage disease: the glomerular size and renal localization of apolipoprotein.
In order to investigate the glomerular size and renal localization of apolipoprotein in type Ia glycogen storage disease, a renal biopsy was performed in two proteinuric patients. Histopathological examination of the biopsy specimens revealed focal sclerotic glomerular sclerosis in both patients. The mean glomerular area was 21.6 +/- 11.6 x 10(3) microns 2, indicating enlargement of the glomeruli. Immunohistochemical staining of the specimens for apolipoprotein showed localization of apolipoprotein AI on the inner side of the glomerular capillary wall, and in proximal tubular epithelial cells. In one patient with a history of several episodes of hypoglycemia, treatment with corn starch improved the carbohydrate and lipid metabolic profile and reduced the daily urinary protein excretion from 2.23 to 0.5 g. These results suggest that focal sclerotic glomerular lesions associated with type Ia glycogen storage disease may be related to disorders of carbohydrate and lipid metabolism.
Adult↗
Autoimmune hemolytic anemia in a patient with polycythemia vera: first description.
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Anemia, Hemolytic, Autoimmune↗