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PubMed1976

Deviated lysis: Transfer of complement lytic activity to unsensitized cells II. Generation of the activity by inulin and by antigen antibody complexes.

Deviated lysis (d.l.) activity, i.e. lysis of unsensitized cells by lytic C activity, was generated via the classical pathway of Cactivation (ag ab complexes) and via the alternative pathway (inulin). The activity was observed on the surface of the activating particles and in the fluid phase. The activity was relatively stable at 32 degrees C. Its generation involved the C components C6 through C9 and possibly also C5.

Animals↗
PubMed1977

Deviated lysis: transfer of complement lytic activity to unsensitized cells. IV. Parital isolation of the activity.

Deviated lysis (d.l.) was previously characterized as the lysis of non-sensitized erythrocytes by activated complement (C) in the presence of EDTA (1, 2, 3). The lytic activity was present in serum fractions of a m.w. in the proximity of 220,000. All the C factors C5 through C9 were found in these fractions and they were all needed for lysis. It is proposed that in d.l. small aggregates of the C components C5 through C9 coexist in the reaction mixture without further interaction. Only when appropriate receptors such as present on target cells surfaces are available, the factors react in a sequential order eventually to result in lysis of the target cell.

Animals↗
PubMed1977

Acute hepatitis: significance of changes in complement components.

Serial measurements of complement components were performed in fifty-nine patients with acute, uncomplicated hepatitis and twelve with alcoholic cirrhosis. Thirty-one of the former group had detectable hepatitis B antigen. Abnormal complement profiles were observed in nine patients with hepatitis B and seven with antigen-negative hepatitis. Low levels of C4, C3 and factor B were common in the subjects with cirrhosis and confined to those cases with severe reduction in serum albumin and/or prothrombin index. By contrast, the complement changes in the patients with hepatitis occurred without significant alteration in these parameters; certain subjects also had reduction in C1q and C5 and a significant number had C3d detectable in fresh plasma. The pattern of abnormality suggests predominant involvement of the classical pathway and it is concluded that this results, at least in part, from an immune process evident only in the early clinical phase of hepatitis. Such gross changes in complement are likely to reflect immune-complex activity and it is proposed that these complexes may be important in the clearance of virus material. The data supports a previous suggestion that recovery from acute hepatitis is primarily dependent on host immune competence rather than viral cytotoxicity or generation of immune complexes.

Acute Disease↗
PubMed1989

Complement C6 and C7 polymorphisms in Japanese patients with chronic glomerulonephritis.

C6 and C7 types were studied in 158 Japanese patients with different types of chronic glomerulonephritis: 75 patients with IgA nephropathy (IgA-N); 49 patients with idiopathic membranous nephropathy (IMN), and 34 patients with minimal-change nephrotic syndrome (MCNS). There were significant differences in the C6 and C7 allele and phenotype frequencies between the patient groups and controls. A strong association was found between IgA-N and C7 5 phenotype (p less than 0.001, RR = 12.71), and between MCNS and C7 5 phenotype (p less than 0.001, RR = 14.20). A significant association between MCNS and C6 B2 phenotype (p less than 0.05, RR = 2.42) was also found. In the IMN patient group, a significant association with C7 4 phenotype (p less than 0.05, RR = 2.42) was observed. Thus, C6 and C7 phenotypes may be causative factors in the development of chronic glomerulonephritis.

Complement C6↗
PubMed1987

Human alveolar macrophages synthesize active complement components C6, C7, and C8 in vitro.

We investigated whether serum-free human alveolar macrophage cultures synthesize active C6, C7, and C8. There was a significant binding of polyclonal anti-human C6 antibodies to agarose beads incubated with unstimulated macrophages for 24 or 48 h. Endotoxin stimulation of the macrophages was necessary for significant binding of polyclonal anti-C7 and anti-C8 antibodies to agarose beads co-cultured for 48 or 96 h. Two monoclonal antibodies (poly C9-MA and MCaE11) specific for a neoantigen of polymerized C9 in the terminal complement complex (TCC), bound to beads mainly incubated with endotoxin stimulated macrophages. The MCaE11 was more sensitive than the poly C9-MA in detecting the C9 neoantigen on beads incubated with the macrophages or human serum diluted 1:16. We thus conclude that human alveolar macrophages synthesize active C6, C7, and C9 that together with C5 and C9, assemble as the TCC on co-cultured agarose beads. Activation of the alternative pathway on the agarose with generation of fixed C3 and C5 convertases is a prerequisite for the subsequent generation of the TCC.

Adult↗
PubMed1991

Functionally active complement proteins C6 and C7 detected in C6- and C7-deficient individuals.

Two sensitive sandwich ELISAs based on monoclonal antibodies directed to native C6 and C7 allowed the detection and quantitation of these complement proteins in 20 out of 37 serum samples from individuals who had previously been classified as deficient in these proteins as assessed by immunochemical and/or functional assays. Furthermore, serum from four C6-deficient and one combined C6-/C7-deficient individual showed an increase in the terminal complement complex (TCC) and a decrease in native C6 and C7 after complement activation as assayed by specific ELISAs. Despite their (incomplete) deficiencies, these individuals therefore possess functionally active terminal complement proteins with respect to their ability to generate the TCC. As these individuals have no history of a susceptibility to neisserial infections, even low concentrations of functionally active C6 and C7 may provide sufficient protection against those micro-organisms whose destruction requires TCC formation.

Antibodies, Monoclonal↗
PubMed1985

Close linkage between mouse genes determining the two forms of complement component C6 and component C7, and cis action of a C6 regulatory gene.

Two forms of mouse complement component C6, with molecular weights (Mrs) of 90 and 100 kilodaltons (kd), are present in the sera from certain inbred strains such as the CBA strain; other strains, such as the BALB/c and DBA/2 strains, have only the 90 kd C6A form. The present work was undertaken to determine whether the two Mr forms were the products of genes coding at separate loci. We screened sera from mice from a number of inbred strains by isoelectric focusing and found one strain, AKR, exhibiting allotypic structural variations of C6 forms. To distinguish the various types, we designated the 90 kd types from CBA and AKR mice C6A1 and C6A2, respectively, and the corresponding 100 kd types C6B1 and C6B2, respectively. Mice possessing only one Mr form were all typed as C6A1. Results of breeding experiments strongly suggested that the two Mr forms of C6 are coded for at two closely linked loci. Sera from a number of inbred strains were also screened for a complement C7 polymorphism by means of isoelectric focusing and functional overlay. C7 from all strains, excepting the AKR strain, produced identical C7 band patterns. AKR C7 produced a unique band pattern, and results of breeding experiments with AKR and BALB/c mice showed the C6 and C7 loci to be closely linked. In addition, we identified a regulatory gene for C6 production. The gene apparently requires androgen to facilitate C6 production in the majority of strains. In these strains C6 activity is virtually absent from female sera. However, we observed moderate levels of C6 activity in sera from IS/Cam females, indicating that, in this strain, male physiological androgen levels are not necessary for C6 production. IS/Cam possess one form of circulating C6 which appears identical with BALB/c C6A1, and therefore IS/Cam mice differ from AKR mice at both the C6 structural and regulatory loci. These two strains were thus suitable for use in breeding experiments to determine the manner of action of the regulatory gene. Results showed that it acted in a cis manner.

Animals↗
PubMed1986

Synthesis of complement components C5, C6, C7, C8 and C9 in vitro by human monocytes and assembly of the terminal complement complex.

Monocytes cultured under serum-free conditions secreted protein which bound covalently and non-covalently to agarose beads, an activator of the alternative pathway of complement. There was a significantly binding of monoclonal anti-C3c antibodies, polyclonal anti-C5, anti-C6, anti-C7, anti-C8, and anti-C9 antibodies, and of a monoclonal antibody against a neoantigen of polymerized C9 to agarose beads incubated with the monocytes for 24, 48, 72 or 96 h. From these results, we conclude that monocytes produce C5, C6, C7, C8 and C9 that assemble as the terminal complement complex on the surface of the agarose beads. Activation by agarose of the alternative pathway with generation of particle bound C3 and C5 convertases is a prerequisite for the subsequent formation of the terminal complement complex. Whether SC5b-9 or the membrane attack of complement (C5b-9) is formed on the beads will be examined.

Antibodies, Monoclonal↗
PubMed1987

[Purpura fulminans associated with a C7 deficiency].

A patient suffering from purpura fulminans was found to have a hereditary deficiency of the C7 component of complement. The homozygous deficiency of late acting complement components increases the risk of neisserial infection. CH50 titration will detect those patients suffering from a homozygous deficiency, who should be vaccinated against Neisseria meningitidis types.

Adolescent↗
PubMed1990

The assignment of the genes coding for human complement components C6 and C7 to chromosome 5.

A panel of 19 somatic cell hybrids was tested for the presence of human sequences coding for complement components C6 and C7 by restriction enzyme digestion and Southern blots probed with human C6 and C7 cDNA probes. C7 was also detected by amplifying part of the human gene in hybrid DNA using the polymerase chain reaction. Detection of human C6 and C7 was completely correlated with the presence of chromosome 5.

Animals↗
PubMed1991

In vitro demyelination by serum antibody from patients with Guillain-Barré syndrome requires terminal complement complexes.

Serum from 7 patients who had acute-phase Guillain-Barré syndrome with high anti-peripheral nerve myelin antibody activity (54 to 210 units/ml) was compared with serum from 3 patients in the recovery phase (0 to 17 units/ml) and serum from 7 disease control subjects (0 to 24 units/ml) and 7 normal control subjects (0 to 7 units/ml) for its ability to demyelinate rodent dorsal root ganglion cultures. The demyelinating capacity of each serum was quantitated by counting the percent of damaged internodal segments in each of four cultures. All sera from patients in the acute phase GBS caused 50 to 78% demyelination, in contrast with 6 to 19% by the sera from all 3 patients in the recovery phase and all other control subjects. The degree of demyelination correlated with anti-peripheral nerve myelin antibody activity of the sera and demyelination was complement-dependent. Further, cultures were treated with an immunoglobulin M (IgM) fraction of an acute-phase Guillain-Barré syndrome plasma plus normal human serum depleted of complement component C7. Only those cultures treated with IgM and C7-depleted human serum reconstituted with purified C7 resulted in 50.8% demyelination, which was significantly greater than the 14.2 to 16.2% demyelination observed in the presence of heat-inactivated, C7-depleted human serum plus purified C7 or in the absence of C7 or antibody. In summary, our work suggests that anti-peripheral nerve myelin antibody in Guillain-Barré syndrome mediated complement dependent-demyelination of rodent dorsal root ganglion cultures. Further, this in vitro demyelination required generation of activation complexes of the terminal complement cascade.

Acute Disease↗
PubMed1976

Increased ion permeability of planar lipid bilayer membranes after treatment with the C5b-9 cytolytic attack mechanism of complement.

The ion permeability of planar lipid bilayers, as measured electrically, was found to increase modestly upon treatment with purified complement complex C5b,6 and complement components C7 and C8. The subsequent addition C9 greatly amplified this change. No permeability changes occurred when components were added individually to the membrane, or when they were used in paired combinations, or when C5b, C7, C8, and C9 were admixed prior to addition. Thus, there is a significant parallel between the permeability changes induced in the model membrane and damage produced in biological membranes by the C5b-9 complement attack sequence. The efficiency of membrane action by C5b-9 was critically dependent on the order in whcih components were added to the membrane. There were also differences in the electrical properties of membranes treated with C5b-8 and C5b-9, though in both cases the enhanced bilayer permeability is best attributed to the formation of trans-membrane channels. Collectively, the data are consistent with the hypothesis that the mechanism of membrane action by complement involves the production of a stable channel across the lipid bilayer, resulting in cell death by colloid-osmotic lysis.

Cell Membrane Permeability↗
PubMed1989

A case of hereditary combined deficiency of complement components C6 and C7 in man.

Immunological investigation of a patient presenting with candidiasis and toxoplasmosis revealed a combined deficiency of C6 and C7. Deficiency of C6 was total, but small amounts (less than 1 microgram/ml) of apparently normal C7 were present in the serum. All family members (three sibs and both parents) were heterozygous for the combined deficiency. This is only the second reported case of combined homozygous deficiency of the closely linked and immunochemically similar proteins C6 and C7, and only the third kindred in which this defect has been demonstrated.

Adult↗