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At least 307 records · Page 17Linked to original sources
PubMed1990

Protection of human amniotic epithelial cells (HAEC) from complement-mediated lysis: expression on the cells of three complement inhibitory membrane proteins.

Cultured human amniotic epithelial cells (HAEC) were found by immunofluorescence microscopy to express three complement inhibitory membrane proteins, CD59 antigen, decay-accelerating factor (DAF) and membrane attack complex (MAC) inhibitory protein (MIP), on their surfaces. The effects of incubation with Fab2 fragments of monoclonal antibodies (mAb) raised against these proteins on susceptibility of sensitized cells to lysis by homologous complement was examined. Percentage cell lysis was markedly increased in the presence of Fab2 anti-CD59 and to a lesser, but significant, extent in the presence of Fab2 anti-DAF. Fab2 anti-MIP did not alter the sensitivity of the cells to lysis by complement.

Amnion↗
PubMed1976

Lysis of tumor cells by antibody and complement. VII. Complement-dependent 86Rb release--a nonlethal event?

The guinea pig hepatoma (line-1) treated with anti-Forssman antibody (TA) and GPC sequentially released 86Rb, 14C from 14C aminoidobutyric acid and failed to exclude trypan blue. Incubation of TA with fluid phase GPC for 1 min caused maximal 86Rb release; however, if the GPC was removed at this time, the cells were not subsequently killed. Using a number of naturally occurring human sera deficient in a complement component we have shown 86Rb release requires the binding of the complement components 1 through 8, but there was no absolute requirement for C9. Irreversible damage to the cell as measured by 14C AIB release or uptake of trypan blue required the complete sequence of complete sequence of complement components. These observations indicate that 86Rb release is not a relible indicator cytotoxicity.

Animals↗
PubMed1984

Complement components, complement activation, and acute phase response in systemic lupus erythematosus.

The investigation concerned 33 systemic lupus erythematosus (SLE) patients assigned to three groups representing mild SLE, more severe extra renal SLE, and SLE with significant renal involvement. In patients with extrarenal disease, the inflammatory plasma protein response was often pronounced during exacerbation, as evidenced by markedly increased concentrations of C-reactive protein (CRP), alpha 1-antichymotrypsin, alpha 1-antitrypsin, and orosomucoid. CRP responses were rare in patients with renal involvement, despite the increased concentrations of other acute-phase reactants in some of these patients. Superimposed bacterial infections were not clearly distinguished by raised CRP concentrations. The classical pathway of complement was activated in all patients during exacerbation, as indicated by increased concentrations of C1r-C1s-C1 inactivator complexes and C2a fragments. C1, C2, and probably also C3 activation varied according to the amounts of circulating C1q-binding immune complexes, as measured by solid-phase assay. Manifest hypocomplementemia was usually associated with glomerulonephritis. Participation of complement components in the inflammatory plasma protein response apparently counteracted the development of hypocomplementemia in many patients with extrarenal SLE. Circulating C3d was detected in all patients during exacerbation of renal disease and in most patients with severe extrarenal manifestations. Inverse relationships were found between immunochemical C2 concentrations and the percentage of cleaved C2 and between C3 and C3d. There was no appreciable consumption of factors B and D and properdin of the alternative pathway in the patients. High concentrations of factor D, a low molecular weight protein, were exclusively found in patients with renal involvement and could be ascribed to retention due to reduced glomerular filtration.

Antigen-Antibody Complex↗
PubMed1984

Structural and functional characterization of the RNA-positive complementation groups, C and D, of the New Jersey serotype of vesicular stomatitis virus: assignment of the M gene to the C complementation group.

The structural and functional lesions in the RNA-positive complementation groups, C and D, of the New Jersey serotype (Hazelhurst subtype) of vesicular stomatitis virus have been characterized. The M protein of the temperature-sensitive mutant C1, the prototype of the C complementation group, was degraded at the restrictive temperature in vivo, and was resolved from the wild-type M protein by SDS-polyacrylamide gel electrophoresis and nonequilibrium pH gradient electrophoresis. Coreversion of these properties and the temperature-sensitive phenotype was observed in a spontaneous revertant. On the basis of these results, the M gene was assigned to the C complementation group. Intracellular nucleocapsids could not be isolated from New Jersey serotype infections by procedures developed for Indiana serotype infections. Therefore, in order to assess the ability of New Jersey ts mutants to accumulate nucleocapsids at the restrictive temperature, a procedure for their isolation was developed. Hypertranscription was observed in C1-infected cells incubated at the restrictive temperature, but was not accompanied by proportionate increases in intracellular viral nucleocapsids or protein synthesis. The G and N proteins of the temperature-sensitive mutant D1, the sole representative of the D complementation group, were electrophoretic variants. The relative yield of intracellular D1 N protein was lower at the restrictive than at the permissive temperature, and the D1 L protein was thermolabile. No intracellular viral nucleocapsids were detected in D1 infected cells incubated at the restrictive temperature; however, more 40 S and less message-sized RNA were synthesized at the restrictive than at the permissive temperature. These results suggested functional defects in both the N protein and polymerase of D1.

Animals↗
PubMed2001

Mutagenesis of apobec-1 complementation factor reveals distinct domains that modulate RNA binding, protein-protein interaction with apobec-1, and complementation of C to U RNA-editing activity.

C to U editing of apolipoprotein B (apoB) RNA requires a multicomponent holoenzyme complex in which minimal constituents include apobec-1 and apobec-1 complementation factor (ACF). We have examined the predicted functional domains in ACF in binding apoB RNA, interaction with apobec-1, and complementation of RNA editing. We demonstrate that apoB RNA binding and apobec-1-interacting domains are defined by two partially overlapping regions containing the NH(2)-terminal RNA recognition motifs of ACF. Both apoB RNA binding and apobec-1 interaction are required for editing complementation activity. ACF is a nuclear protein that upon cotransfection with apobec-1 results in nuclear colocalization and redistribution of apobec-1 from the cytoplasm. ACF constructs with deletions or mutations in the putative nuclear localization signal (NLS) still localize in the nucleus of transfected cells but do not colocalize with apobec-1, the latter remaining predominantly cytoplasmic. These observations suggest that the putative NLS motif in ACF is not responsible for its nucleo-cytoplasmic trafficking. By contrast, protein-protein interaction is important for the nuclear import of apobec-1. Taken together, these data suggest that functional complementation of C to U RNA editing by apobec-1 involves the NH(2)-terminal 380 residues of ACF.

APOBEC-1 Deaminase↗
PubMed1984

Complement-mediated solubilization of immune complexes. Solubilization inhibition and complement factor levels in SLE patients.

Thirty-two of 36 serum samples from 19 SLE patients showed reduced capacity to mediate complement-dependent solubilization of immune complexes (IC). SLE patients with nephritis exerted the lowest complement-mediated solubilization capacity (CMSC) whereas sera from patients with inactive disease gave the highest CMSC values, with three out of four samples within the normal reference range. Thirty-five of the 36 serum samples showed inhibition of CMSC in a newly developed CMSC inhibition assay. The strongest CMSC inhibition was exerted by sera from newly discovered cases of SLE who received no medical treatment and the lowest inhibition by sera from patients with inactive disease. There was a significant negative correlation between CMSC and CMSC inhibition (r = -0.67, P less than 0.001). Sera with low concentrations of C1q, C3, factor B or high C3d levels showed markedly reduced CMSC values. Pronounced CMSC inhibition was observed only in samples with normal or high factor H values. No significant correlation was found between CMSC or CMSC inhibition and circulating IC levels, but pronounced CMSC inhibition was registered only in strongly IC positive sera.

Adolescent↗
PubMed2002

Complement and dilated cardiomyopathy: a role of sublytic terminal complement complex-induced tumor necrosis factor-alpha synthesis in cardiac myocytes.

Dilated cardiomyopathy is a syndrome characterized by cardiac enlargement and impaired systolic function of the heart. Tumor necrosis factor (TNF)-alpha, a pleiotropic cytokine, seems to play a central role in the progression of dilated cardiomyopathy. Recent data suggest that ongoing inflammation in the myocardium may, in many cases, contribute to the development of disease. Chronic generation of autoantibodies to myocardial antigens or, in some cases, viral infection are pathobiologically involved. Although both antibodies and some viruses activate the complement system, the role of innate immunity in dilated cardiomyopathy has as yet not been investigated systematically. In this study we demonstrate by analysis of myocardial biopsies from 28 patients that C5b-9, the terminal membrane attack complex of complement, accumulates in human myocardium in dilated cardiomyopathy. C5b-9 significantly correlates with immunoglobulin deposition and myocardial expression of TNF-alpha. In vitro, C5b-9 attack on cardiac myocytes induces nuclear factor (NF)-kappaB activation as well as transcription, synthesis, and secretion of TNF-alpha. We conclude that chronic immunoglobulin-mediated complement activation in the myocardium may contribute in part to the progression of dilated cardiomyopathy via C5b-9-induced TNF-alpha expression in cardiac myocytes.

Animals↗
PubMed1984

Kinetics of polymerization of a fluoresceinated derivative of complement protein C9 by the membrane-bound complex of complement proteins C5b-8.

The fluorescence self-quenching by energy transfer of FITC-C9, a fluoresceinated derivative of human complement protein C9 [Sims, P.J. (1984) Biochemistry (preceding paper in this issue)], has been used to monitor the kinetics of C9 polymerization induced by the membrane-associated complex of complement proteins C5b-8. Time-based measurements of the fluorescence change observed during incubation of FITC-C9 with C5b-8-treated sheep red blood cell ghost membranes at various temperatures revealed that C9 polymerization induced by the C5b-8 proteins exhibits a temperature dependence similar to that previously reported for the complement-mediated hemolysis of these cells, with an Arrhenius activation energy for FITC-C9 polymerization of 13.3 +/- 3.2 kcal mol-1 (mean +/- 2 SD). Similar measurements obtained with C5b-8-treated unilamellar vesicles composed of either egg yolk phosphatidylcholine (egg PC), dipalmitoylphosphatidylcholine (DPPC), or dimyristoylphosphatidylcholine (DMPC) revealed activation energies of between 20 and 25 kcal mol-1 for FITC-C9 polymerization by C5b-8 bound to these membranes. Temperature-dependent rates of C9 polymerization were observed to be largely unaffected by the phase state of membrane lipid in the target C5b-8 vesicles. The significance of these observations of the mechanism of C9 activation of membrane insertion is considered.

Animals↗
PubMed2000

The enhancing role of complement in human immunodeficiency virus infection: soluble recombinant CR1 (CD35) inhibits complement-mediated enhancement of infection of a CD4-positive T-cell line with human immunodeficiency virus-1.

The present study investigated the effect of soluble recombinant CR1 (srCR1, sCD35) on complement-dependent enhancement of human immunodeficiency virus-1 (HIV-1) infection in vitro. Cells of the human T-cell line HPB-ALL were infected with HIV-1 that had been preopsonized with normal human HIV-seronegative serum in the presence of srCR1. At nanomolar concentrations, srCR1 suppressed complement-dependent enhancement of infection of HPB-ALL cells in a dose-dependent manner. Under these conditions, infection was decreased to levels similar to those observed in cells infected with unopsonized virus. These observations provide further evidence to support the role of complement-dependent opsonization facilitating viral entry into target cells.

CD4-Positive T-Lymphocytes↗
PubMed1991

Intersection of the complement and immune systems: a signal transduction complex of the B lymphocyte-containing complement receptor type 2 and CD19.

The complement system augments the humoral immune response, possibly by a mechanism that involves the B lymphocyte membrane receptor, CR2, which binds the C3dg fragment of C3 and triggers several B cell responses in vitro. The present study demonstrates that CR2 associates with a complex of membrane proteins that may mediate signal transduction by ligated CR2. Monoclonal antibodies to CR2 immunoprecipitated from digitonin lysates of Raji B lymphoblastoid cells a membrane complex containing CR2, approximately equimolar amounts of CD19, which is a member of the immunoglobulin superfamily, and three unidentified components: p130, p50, and p20. The complex, which was immunoprecipitated also with anti-CD19, could be dissociated by Nonidet P-40, accounting for its absence in previous studies of CR2. Expression of recombinant CR2 and CD19 in K562 erythroleukemia cells led to formation of a complex that contained not only these two proteins but also p130, p50, and p20, and another component, p14. These unidentified components of the CR2/CD19 complex coimmunoprecipitated with CD19 and not with CR2 from singly transfected cells, indicating primary association with the former. CD19 replicated the capacity of CR2 to interact synergistically with mIgM for increasing free intracellular Ca2+, suggesting that the complex mediates this function of CR2. Therefore, CR2 associates directly with CD19 to become a ligand-binding subunit of a pre-existing signal transduction complex of the B cell that may be representative of a family of membrane protein complexes. This interaction between the complement and immune systems differs from that between immunoglobulin and Clq by involving membrane rather than plasma proteins, and by having complement involved in the afferent phase of the immune response.

Antigens, CD↗
PubMed1989

The IgG subclass pattern of complement activation depends on epitope density and antibody and complement concentration.

Using a matched series of human-mouse chimaeric IgG anti-5-iodo-4-hydroxy-3-nitrophenacetyl (anti-NIP) antibodies and NIP-bovine serum albumin (NIP-BSA) we examined how different variables influence the activation pattern of complement. When BSA was used with different hapten densities and the input of NIP-BSA was altered, we observed a change in the subclass reaction pattern. IgG3 fixed more Clq than IgG1 and IgG2 in all situations. IgG1 was slightly better than IgG3 and IgG2 at high antigen concentrations at activating C4 and C3 and inducing formation of the terminal complement complex (TCC). When the epitope density and/or the NIP-BSA concentration was reduced, IgG3 became best, followed by IgG1 and IgG2. IgG1 now revealed a marked prozone. Furthermore, IgG4 was found to activate C3 and mediate TCC formation at high epitope and complement concentrations.

Antibodies↗
PubMed1989

Assessment of the activation pathways of the complement in psoriatic patients by use of complement fragment C4d and Bb measurements.

We have measured the complement fragment C4d and Bb levels in the plasma of 51 psoriatic patients and 54 normal controls. The C4d and Bb levels were not significantly elevated in the plasma of the psoriatic patients when compared with those of controls, except in patients with more than 60% skin involvement who exhibited an increase in Bb levels. C4d levels, however, did decrease slightly after successful treatment of psoriasis. Although these results suggest that the C4d and Bb levels partly reflect the complement activation in vivo, they do not seem to be suitable parameters to clarify the mechanism of complement activation in psoriasis.

Adolescent↗
PubMed1981

The effect of vitamin C deficiency on complement systems and complement components.

The changes in the complement systems and complement hemolytic activities through classical and alternative pathways, and the individual components, C1, C4, C2 and C3 were demonstrated in the course of vitamin C deficiency in guinea pigs. During the course of vitamin C deficiency during the first week after the start of the experiment, all components except C1 slightly decreased, gradually increasing in the following weeks. This indicates that this period is important in the formation of an immune defence system in the host. At the time the symptoms of vitamin C deficiency appeared, C1, C2 and CH50 started to decrease. C3 increased when vitamin C deficiency became severe and showed a completely different pattern from those of the other components. The lowered C1 will be due to a collagen-like region in the characteristic of Clq subcomponent, since insufficient vitamin C state produces impaired collagen formation. The activity of the alternative pathway did not produce any change in this course, even in the severe stage. This indicates that the increase in C3 will contribute to maintaining the level of the alternative pathway and maintaining the body defence system in the vitamin D-deficient state, and that the complement system will be supported through the alternative pathway.

Animals↗
PubMed2003

Expression of complement 3 and complement 5 in newt limb and lens regeneration.

Some urodele amphibians possess the capacity to regenerate their body parts, including the limbs and the lens of the eye. The molecular pathway(s) involved in urodele regeneration are largely unknown. We have previously suggested that complement may participate in limb regeneration in axolotls. To further define its role in the regenerative process, we have examined the pattern of distribution and spatiotemporal expression of two key components, C3 and C5, during limb and lens regeneration in the newt Notophthalmus viridescens. First, we have cloned newt cDNAs encoding C3 and C5 and have generated Abs specifically recognizing these molecules. Using these newt-specific probes, we have found by in situ hybridization and immunohistochemical analysis that these molecules are expressed during both limb and lens regeneration, but not in the normal limb and lens. The C3 and C5 proteins were expressed in a complementary fashion during limb regeneration, with C3 being expressed mainly in the blastema and C5 exclusively in the wound epithelium. Similarly, during the process of lens regeneration, C3 was detected in the iris and cornea, while C5 was present in the regenerating lens vesicle as well as the cornea. The distinct expression profile of complement proteins in regenerative tissues of the urodele lens and limb supports a nonimmunologic function of complement in tissue regeneration and constitutes the first systematic effort to dissect its involvement in regenerative processes of lower vertebrate species.

Amino Acid Sequence↗
PubMed1977

Measurement of hemolytic complement and the third component of complement in nonhuman primates.

Complement, determined by hemolytic assay, and the third component of complement (C3), determined by radial immunodiffusion assay, were measured in nine nonhuman primate species. The species studied were the titi (Callicebus mollach). The sooty mangabey (Cercocebus atys), the thick-tailed galago or bushbaby (Galago crassicaudatus panganiensis), the crab-eating monkey (Macaca fascicularis), the rhesus monkey (Macaca mulatta), the bonnet monkey (Macaca radiata), the stumptailed macaque (Macaca speciosa), the yellow baboon (Papio cynocephalus), and the black-and-red tamarin (Saguinus nigricollis). Both sheep and bovine erythrocytes were used in the hemolytic complement assays. With the sheep erythrocyte system, sera from four species (yellow baboon, sooty mangabey, bonnet monkey, black-and-red tamarin) had similar titers with both antibody sensitized and non-sensitized erythrocytes. In contrast, the titers obtained using sensitized bovine erythrocytes was always higher than the values obtained using non-sensitized bovine erythrocytes. In all species, the titers for non-sensitized sheep erythrocytes was higher than the titer for non-sensitized bovine erythrocytes. When the species were compared for cross reactivity using the radial immunodiffusion assay for human C3, the rhesus monkey showed the strongest cross reaction; the thick-tailed galago, a prosimian, showed no detectable cross reactivity; and the other species examined showed intermediate degrees of reactivity.

Animals↗
PubMed1984

[Activation of the alternative complement pathway by Newcastle disease virus. I) Effect of the virus on the complement system in vivo and in vitro].

The authors have studied the effect of the paramyxovirus of Newcastle disease on the complement system in the mouse. The results obtained show that NDV activate both in vivo and in vitro the alternative complement pathway, suggesting that the intervention of complement system during viral infections represents a general biological phenomenon.

Animals↗
PubMed1980

Experimental bovine trypanosomiasis (Trypanosoma vivax and T. congolense). II. Serum levels of total protein, albumin, hemolytic complement, and complement component C3.

Serum levels of total protein, albumin, activity of hemolytic complement, and complement component C3 were decreased in cattle infected with either T. congolense or T. vivax. The hemolytic complement activity was reduced most, i.e. to 20% (T. congolense) or 5% (T. vivax) of control levels. The development of hypocomplementemia was closely associated with the first peak of parasitemia.

Animals↗