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PubMed1993

Complement activation and C3 allotype distribution in patients with bronchial asthma.

61 patients suffering from intrinsic (idiotypic) or extrinsic (allergic) asthma were investigated for signs of complement activation and for C3 phenotype distribution. Activation of both the classical and alternative pathway of the complement system and generation of the membrane attack complex could be assessed by ELISAs for the activation-specific protein-protein complexes C1rsC1 inhibitor, C3b(Bb)P and SC5b-9, respectively. A possible deficiency of the complement regulatory proteins C1 inhibitor, factor H and factor I was excluded. In contrast to earlier studies, C3 allele frequencies did not differ from those found in the healthy population. Our results support the role of complement activation during bronchial asthma and, thereby, provide further evidence for the inflammatory nature of the disease.

Alleles↗

PubMed1991

Expression of a soluble and functional form of the human beta 2 integrin CD11b/CD18.

Polymorphonuclear cells and monocytes (phagocytes) are a critical component of host defense against infections. However, these cells also play a significant role in host tissue damage in many noninfectious diseases, such as ischemia-reperfusion injury syndromes and rejection of transplanted organs. The leukocyte adhesion molecule family CD11/CD18 (beta 2 integrins) is critical to the function of polymorphonuclear cells and monocytes in inflammation and injury. Inherited deficiency of CD11/CD18 impairs phagocyte chemotaxis, adhesion and transmigration across endothelium, and clearance of invading microorganisms through phagocytosis and cell-mediated killing. Furthermore, murine monoclonal antibodies directed against the CD11b/CD18 (CR3) heterodimer have been shown to reduce, by 50%-80%, phagocyte-mediated ischemia-reperfusion injury in several organ systems, such as the myocardium, liver, and gastrointestinal tract and to inhibit development of insulin-dependent diabetes mellitus in nonobese diabetic (NOD) mice. Expression of CD11b/CD18 in a soluble and functional form might therefore be potentially useful as an anti-inflammatory agent. We have now expressed a recombinant soluble heterodimeric form of this human beta 2 integrin, normally expressed as two noncovalently associated membrane-bound subunits. The secreted receptor exhibited direct and specific binding to its ligand, iC3b, the major complement C3 opsonin, and inhibited binding of polymorphonuclear cells to recombinant interleukin 1-activated endothelium.

Amino Acid Sequence↗

PubMedDate not supplied

[Levels of the individual complement components in the blood serum of volunteers on diets with a various levels of optimal protein composition].

Protein fractions of complement (C3, C4, C5 and C9) and the control protein Ct-inhibitor) were studied in blood serum of practically healthy men placed on the diet marked by protein deficiency. It was noted that C3 and C9 were particularly sensitive to protein deficiency in the diet (5 to 8.2 g/day according to nitrogen), with the titers of these fractions being low.

Complement System Proteins↗

PubMed1978

Localized heat urticaria.

The pathophysiology of localized heat urticaria was studied by performing a heat challenge on a patient with this disease. Serum levels of total hemolytic complement, C3, and factor B decreased following heat challenge, whereas levels of C4 and C5 did not. Plasma histamine levels remained unchanged. Electron microscopic studies of affected tissue revealed endothelial cell damage and neutrophilic degranulation in the affected area. Mast cells remained intact. These data imply that activation of the alternative complement pathway is involved in the pathogenesis of localized heat urticaria and that mast cell histamine release does not play a significant role in this disease.

Adult↗

PubMed1986

The role of complement in monoclonal antibody-mediated protection against virulent Semliki Forest virus.

Monoclonal antibodies (MAs), specific for either the E1 or E2 glycoproteins of Semliki Forest virus (SFV), and belonging to various immunoglobulin subclasses (IgM, IgG2a, IgG2b and IgG3), effected lysis of SFV-infected L cells in co-operation with guinea-pig complement. In this antibody-dependent complement-mediated cytolysis (ADCMC) test, IgG1 MAs were not effective although these antibodies recognize the viral antigens on the surface of SFV-infected L cells. The latter was shown with horseradish peroxidase (HRPO)-labelled MAs in a direct enzyme immunoassay. The binding reactivities of HRPO-labelled MAs to infected L cells at selected time-intervals after infection correlated well with the amount of cytolysis in a parallel ADCMC test. Cytolysis was dependent on the duration of incubation with antibodies: more cytolysis was measured after a 4-hr incubation period with MA, starting at 4 hr after infection, compared to a 1-hr incubation period starting after 7 hr of infection. However, in the latter case (1-hr period) the amount of cytolysis measured correlated better to neutralization and/or protection by MAs than after the extended period (4 hr) of incubation. Complement (C3) depletion by cobra venom factor treatment led to a higher mortality and viraemia of mice prophylactically injected with critically protective doses of either the neutralizing MA UM 8.4 (IgM) or the non-neutralizing MA UM 4.2 (IgG2a). The results suggest a co-operative role of MA with complement in mediating protection against SFV. Passive immunization by administration of low amounts (0.1 micrograms/mouse) of neutralizing MA UM 5.1 resulted in protection of normal mice against a lethal infection with SFV. Mice immunosuppressed by cyclophosphamide were not protected by these doses. If the doses were increased however, these mice were protected both prophylactically and therapeutically. These results indicate that, using critical doses of MAs, an intact immune system ensures survival in normal mice after infection with virulent SFV.

Animals↗

PubMed1984

Functional characteristics of the macrophage receptors for IgG-Fc and C3: failure to detect C3 receptor-mediated extracellular cytolysis by mouse peritoneal macrophages.

The ability of several immunologic ligands to mediate extracellular cytolysis of sheep erythrocytes (E) by mouse macrophages was studied. E coated with rabbit IgG (EIgG), but not nonsensitized E or E coated with rabbit IgM (EIgM), were lysed and phagocytized by resident peritoneal macrophages as well as by macrophages activated in vivo with either BCG or Corynebacterium parvum or in vitro with lymphokine. EIgM incubated with mouse serum to deposit the third component of complement (C3) onto E (EIgMC) were ingested by thioglycolate-elicited and lymphokine-treated macrophages, but not by the other macrophage populations examined. However, none of the macrophages performed lysis of EIgMC, suggesting that engagement of macrophage C3 receptors by target cell-bound C3 was not a sufficient trigger for cytolysis. Lysis of E coated with both IgG and C3 (EIgGC) was moderately elevated over that of EIgG; this enhancement was not abolished after proteolytic destruction of the macrophage C3-rosetting capacity, indicating that C3 receptors were not responsible. EIgGC and EIgMC were more susceptible to hypotonic lysis than were either E, EIgG, or EIgM, suggesting that enhanced lysis of serum-treated E may be partially explained by increased E fragility.

Animals↗

PubMed2002

Complement's participation in acquired immunity.

The preliminary evidence for the involvement of complement in promoting primary humoral responses dates back over a quarter of a century. However, it is only in the course of the past decade or so that the detailed mechanisms underlying complement's influence have been characterized in depth. It is now clear that complement serves as a regulator of several B cell functions, including specific antibody production, antigen uptake, processing and presentation, and shaping of the B cell repertoire. Of key importance, in this respect, is the role played by the B cell-signaling triad consisting of the B cell receptor for antigen (BCR), a complex composed of the iC3b/C3d fragment-binding complement type 2 receptor (CR2, CD21) and its signaling element CD19 and the IgG-binding receptor FcgammaRIIb (CD32). The positive or negative outcome of signaling through this triad is determined by the context in which antigen is seen, be it alone or in association with natural or induced antibodies and/or C3-complement fragments. The aim of this review is to describe the present status of our understanding of complement's participation in acquired immunity and the regulation of autoimmune responses.

Animals↗

PubMed1974

Acute immunologic pulmonary alveolitis.

Acute immunologic injury of rat lung has been induced by the intrabronchial injection of heterologous antibody and the intravenous injection of radiolabeled antigen. Within 4 h an acute hemorrhagic neutrophil-rich exudate develops in alveolar and interstitial areas and then gradually fades. Lung injury in this model can be quantitated by measurements of increased vascular permeability and extractable hemoglobin. By the use of immunofluorescent techniques, alveolar and interstitial deposits of antigen and antibody have been demonstrated, but not the third component of complement (C3). Although not found in relation to immune complexes, C3 is nevertheless present in damaged lung as measured by accumulation of radiolabeled C3 from the circulation. Ablation experiments indicate the requirement for both circulating neutrophils and C3 for the development of lung injury. These studies provide definition for the development of lung damage induced by immune complexes.

Animals↗

PubMed1990

Serum haemolytic complement activity and C3 levels in bovine trypanosomosis under natural conditions of challenge--early indications of individual susceptibility to disease.

Twenty-five Baoule (Bos taurus) and 12 Zebu (Bos indicus) cattle, which were part of an experiment aimed at characterizing cattle for resistance to trypanosomosis under natural challenge in Burkina Faso, were monitored for complement levels. Total haemolytic activity of the alternative complement pathway and C3 in sera taken weekly were estimated. The results were analysed in relation to the course of the disease, parasitological data, packed red cell volume (PCV) and body weight. All the animals became infected with Trypanosoma vivax and/or T. congolense. The Zebu had to be treated with Berenil (Diminazene aceturate, Hoechst, W. Germany) after a mean period of 5 weeks of infection, whereas 7 of the 25 Baoule remained in good condition throughout the experiment. The remaining 18 Baoule required treatment after a variable period of infection. There was a decrease in haemolytic complement activity (HC') as well as in C3 levels, which coincided with the first detection of parasites in the blood. The titres in the Zebu fell to 10-20% of pre-infection level within 2-3 weeks and they showed no tendency towards regaining normal levels. The drop in complement in the Baoule was less pronounced and was in most cases followed by an increase approaching normal values. In these animals, the complement level in early infection was found to depend on the intensity of parasite load and on the control potential of each individual. There was a significant correlation between minimum complement activity (min. HC'), minimum C3 (min C3) and minimum PCV (min.PCV) in early infection. These three parameters correlated with individual resistance and might, therefore, be useful criteria for the identification of the most resistant individuals within a trypanotolerant breed.

Animals↗

PubMed1989

Binding of complement components C1q, C3, C4 and C5 to a model immune complex in ELISA.

When normal human serum is added to microELISA plates coated with monomeric or aggregated IgG various complement components become bound and can be detected with specific chicken anti-C1q, anti-C3, anti-C4 and anti-C5 antibodies. Using such assays we found increased C1q- and decreased C3- and C4-binding in sera from patients with SLE. In contrast, sera from patients with rheumatoid arthritis showed decreased C3 binding but normal C1q binding. The decreases in C3 and C4 binding observed in the sera from patients with SLE were larger than the corresponding decreases determined by radial immunodiffusion. Comparing these results with those of the CH50 assay, the correlation coefficient between CH50 and the C3-binding assay was 0.48. There was no correlation between the results of the CH50 and those of the C1q-, C4- or C5-binding assays.

Antigen-Antibody Complex↗

PubMed1976

Glomerulonephritis due to Staphylococcus aureus antigen.

Staphylococcus aureus antigen was identified within the glomeruli of a patient with acute bacterial endocarditis and diffuse glomerulonephritis. Routine immunofluorescence had revealed only granular deposits of complement (C3). C3 activator and C4 were not present. Direct immunofluorescence studies with a specific anti-Staphylococcus aureus conjugate were positive. Electron microscopy showed subepithelial and intramembranous electron-dense deposits. Eluates of the kidney did not contain anti-S. aureus antibody. The absence of immunoglobin suggests that the toxic action of S. aureus antigens may activate complement and cause glomerular injury and that immune complexes are not essential for the production of glomerulonephritis in this entity.

Adult↗

PubMed1993

[The effect of heroin on red cell immunoadherence function of human body].

Red cell immunocompetence was studied in 38 cases of heroin addicts by measuring the rate of red blood cell C3b receptor rosette (RBC-C3bRR), and red blood cell immune complex rosette (RBC-ICR) the concentration of complement C3 and the content of circulating immune complex (CIC). The results showed that the rate of RBC-C3bRR and RBC-ICR and C3 concentration in the heroin addicts decreased significantly, while their CIC content increased significantly as compared with those of the controls. It was also found that the duration of drug taking was related with the changes of the rate of RBC-C3bRR and RBC-ICR, C3 concentration and CIC content. It is suggested that red cell immunoadherence function in heroin addicts decreases significantly as to influence the clearance of CIC.

Adolescent↗

PubMed1981

Antibody-mediated enhancement of disease in feline infectious peritonitis: comparisons with dengue hemorrhagic fever.

Non-immune kittens passively immunized with feline serum containing high-titered antibodies reactive with feline infectious peritonitis virus (FIPV) developed a more rapid disease after FIPV challenge than did kittens pretreated with FIPV antibody-negative serum. Antibody-sensitized, FIPV challenged--kittens developed earlier clinical signs (including pyrexia, icterus, and thrombocytopenia) and died more rapidly than did non-sensitized, FIPV-challenged kittens. Mean survival time in sensitized kittens was significantly (P less than 0.05) reduced compared to non-sensitized kittens (mean +/- SEM, 10.0 +/- 0.6 days vs. 28.8 +/- 8.3 days, respectively). Lesions induced included fibrinous peritonitis, disseminated pyogranulomatous inflammation and necrotizing phlebitis and periphlebitis. FIPV antigen, immunoglobulin G, complement (C3) and fibrinogen were demonstrated in lesions by immunofluorescence microscopy. The pathogenesis of dengue hemorrhagic fever (DHF) in persons bears striking resemblance to that of FIP in experimental kittens. In both FIP and DHF, non-neutralizing antibody may promote acute disease by enhancement of virus infection in mononuclear phagocytes or by formation of immune complexes, activation of complement and secondary vascular disturbances.

Animals↗

PubMed1985

Glomerular C3b receptor loss in renal allografts.

There is almost no data from the glomeruli of allografted kidneys with respect to changes in the CR-1 (C3b) receptor expressed on glomerular podocytes. We studied 22 renal graft biopsies from rejecting and stable allografts, using a panel of monoclonal antibodies. We found that the CR-1 expression was decreased in a focal and segmental fashion in some biopsies, particularly in rejecting kidneys. These changes correlated with the intensity of glomerular mononuclear cell infiltration, but in contrast no correlation was seen with peripheral capillary wall deposition of complement (C3). Thus, some active process is occurring in the glomeruli of rejecting grafts which affects the expression of the CR-1 receptor.

Graft Rejection↗

PubMed1998

A conserved element in the serine protease domain of complement factor B.

Factor B and C2 are serine proteases that carry the catalytic sites of the complement C3 and C5 convertases. Their protease domains are activated by conformational changes that occur during convertase assembly and are deactivated upon convertase dissociation. Factor B and C2 share an 8-amino acid conserved sequence near their serine protease termini that is not seen in other serine proteases. To determine its importance, 24 factor B mutants were generated, each with a single amino acid substitution in this region. Whereas most mutants were functionally neutral, all five different substitutions of aspartic acid 715 and one phenylalanine 716 substitution severely reduced hemolytic activity. Several aspartic acid 715 mutants permitted the steps of convertase assembly including C3b-dependent factor D-mediated cleavage and activation of the high affinity C3b-binding site, but the resulting complexes did not cleave C3. Given that factor B and C2 share the same biological substrates and that part of the trypsin-like substrate specificity region is not apparent in either protein, we propose that the conserved region plays a critical role in the conformational regulation of the catalytic site and could offer a highly specific target for the therapeutic inhibition of complement.

Amino Acid Sequence↗

PubMed1986

Agglutination of sheep erythrocyte-rabbit antibody complexes treated with sheep serum by a rabbit antiserum specific for the third component (C3) of sheep complement.

Sheep E-rabbit A incubated with sheep serum for up to 20 min at 39 degrees C and washed were agglutinated by a rabbit antiserum (anti-inulin-foetal lamb serum) that was specific for sheep C3. If incubated for longer than 20 min at 39 degrees C, there was less sensitisation. Such a complex was not readily generated at 17 degrees C whereas there was no reaction if incubated at 2 degrees C. Once the sheep E-rabbit A-sheep C complex had been generated at 39 degrees C and washed free of sheep serum, it could still be agglutinated after overnight storage at 4 degrees C. Addition of chelators of Ca2+ and/or Mg2+ or antrypol or cobra venom factor (a specific inhibitor of C3) prevented sensitisation of sheep E-rabbit A by sheep serum for agglutination. These results show that sheep serum C3 was taken up by sheep E-rabbit A and its presence on this indicator demonstrated by agglutination using a rabbit antiserum specific for sheep C3.

Animals↗

PubMed2006

Peripheral blood lymphocyte apoptosis and circulating dendritic cells in patients with systemic lupus erythematosus: correlation with immunological status and disease-related symptoms.

We investigated in vivo the relationship between the degree of peripheral blood lymphocyte apoptosis and circulating dendritic cells (DC) as well as the immunological status in 45 patients with systemic lupus erythematous (SLE). Apoptosis was detected by phosphatidylserine externalization and assays to detect caspase activation. The total DC count (tDC) and their myeloid, mDC1 (BDCA1+) and mDC2 (BDCA3+), and plasmacytoid, pDC (BDCA3+), subtypes were assessed. Moreover, several immunological parameters, such as complement proteins, interferons (IFN), tumor necrosis factor (TNF)-alpha, interleukin (IL)-4, and IL-6 levels were assessed. There were no significant differences in both the intensity of apoptosis and DC counts between active and inactive SLE as well as between untreated patients and those treated with steroids. The incidence of lymphocyte apoptosis correlated positively with T-cell count, both T-helper (p=0.004) and cytotoxic T cells (p=0.001), but not with B or natural killer (NK) cells. The intensity of apoptosis enhanced along with the increase in complement C3 (p=0.016) and decrease in IFN-gamma (p=0.040) levels. The apoptotic cell count correlated with tDC (p=0.031), mDC1 (p=0.007), and pDC (p=0.039) counts. Both tDC and mDC1 counts correlated positively with antinuclear antibody (ANA) titers (p=0.017 and 0.032, respectively). Moreover, tDC correlated with C4 (p=0.039) and pDC with both C3 (p=0.032) and C4 (p=0.007) levels. The DC counts correlated inversely with IFN-gamma (tDC, p=0.038; mDC1, p=0.009), IL-6 (mDC2, p=0.031), or serum IgG levels (tDC, p=0.006; mDC1, p<0.001; mDC2, p=0.001). We found a positive correlation between lymphocyte apoptosis and peripheral blood DC count as well as the level of complement proteins in patients with SLE. The enhanced lymphocyte apoptosis was accompanied by the decrease in concentration of some cytokines, such as IFN-gamma or IL-6, as well as serum IgG level. This finding may reflect pathogenetic events during development of the disease, which include a persistent signal derived from circulating apoptotic lymphocytes, mobilizing the complement system, and attracting peripheral blood DC.

Adult↗

PubMed1985

Circulating IgA immune complexes in AIDS.

Circulating immune complexes were isolated from the serum of patients with AIDS, as well as patients with other acute and chronic viral diseases. Analysis of these immune complexes by methods of flow cytometry and by radioimmune (Raji cell) assay revealed a prevalence of IgA complexes in the serum of AIDS patients and a prevalence of IgG complexes in the serum of patients with other viral diseases. Raji cells bind immune complexes via Fc and complement (C3) receptors and may detect IgA immune complexes more efficiently than a C1q assay since IgA has no affinity for C1q.

Acquired Immunodeficiency Syndrome↗