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PubMed1981

Screening for deficiencies in the classical and alternative pathways of complement by hemolysis in gel.

Two assays based on hemolysis in gel were assessed for screening complement (C) component deficiencies. In one assay sensitized sheep erythrocyte (EA) were incorporated in agarose gel containing Ca2+ and Mg2+, in the other guinea pig erythrocytes (GpE) were used in the presence of Mg2+and EGTA. With few exceptions, fresh samples from healthy individuals produced homogeneous areas of complete hemolysis in both assays. Clearly aberrant patterns were observed in approximately 4% of healthy blood donors. Sera from patients having complete deficiencies of Clq, C2 or C4 produced clear lysis of GpE only, whereas in sera lacking C3 or C8 lysis was grossly impaired in both assays. Properdin deficient serum produced very slight lysis of GpE but normal lysis of EA. Reconstitution of these C-deficient sera gave normal lysis. Together, the two assays supplement immunochemical C3 and C4 determinations for screening out C disorders.

Animals↗
PubMed1981

C1q binding and complement activation by capsular and cell wall components of S. pneumoniae type XIX.

Cell wall components (purified cell walls, teichoic acid and residual cell walls) from S. pneumoniae type XIX showed antibody independent C1q binding capacity, as assessed by C1q deviation test, with teichoic acid being the most efficient. Specific capsular substance did not bind C1q. All substances tested produced C1 activation in normal human serum, but not in hypo-gamma-globulinemic serum. Thus, teichoic acid showed high C1q binding capacity but did not activate C1 in the absence of antibodies. Teichoic acid was an effective activator of alternative pathway. Specific capsular substance did not activate the alternative pathway in C1q deficient serum or in Mg2+ -EGTA chelated normal serum.

Cell Wall↗
PubMed1983

Complement-binding antibodies to Aspergillus fumigatus in patients with pulmonary aspergillosis.

Complement-binding antibodies against Aspergillus fumigatus were determined by a fluorescent antibody technique with purified human Clq as the source of complement. Clq binding aspergillus antibodies were found in 8 (67%) of 12 patients with pulmonary aspergillosis, in 4 (57%) of 7 patients with suspected pulmonary aspergillosis, in one (14%) of 7 patients with precipitating antibodies to A. fumigatus of undetermined clinical significance, and in 4 (7%) of 54 healthy blood donors. Sera from patients with definite or probable aspergillosis produced an immunofluorescent staining of hyphal cytoplasm, whereas the staining obtained with positive donor sera was confined to hyphal walls. A positive correlation was found between the frequency and titres of Clq binding antibodies and titres of IgG and IgM aspergillus antibodies. Clq binding antibodies were found only in sera with an IgG aspergillus antibody titre greater than or equal to 640. The frequency of Clq binding antibodies in sera with IgG titres greater than or equal to 640 was significantly higher in patients with aspergillosis (67%) than in blood donors (16%) (p = 0.0036). The Clq binding antibody test may provide diagnostic information as well as clues to the pathogenesis of aspergillus lung disease.

Adolescent↗
PubMed1986

Interaction of purified lipoteichoic acid with the classical complement pathway.

Glycerophosphate-containing lipoteichoic acids (LTAs) interact with the first component of the classical complement pathway (C1). This resulted in the activation of the classical complement pathway in serum, shown by the consumption of C1, C2, and C4. The dose-dependent interaction of LTAs with purified C1 and C1q was dependent on the negative charges of the phosphate groups of LTA. It was reduced by charge compensation through D-alanine ester substituents and by sterical hindrance through di- and trihexosyl residues linked to position 2 of the glycerol moieties. The charge density of LTA may also play a role: poly(digalactosylglycerophosphate) LTAs, in which the phosphate groups are in a greater distance from each other, were less effective, and the loss of micellar organization by deacylation of LTA drastically reduced the complement activation capacity.

Complement Activating Enzymes↗
PubMed1982

Defective yeast opsonisation and functional deficiency of complement in sickle cell disease.

Opsonisation of heat-killed baker's yeast, functional activity of the total alternative pathway of complement, and factor B detected functionally and immunochemically were significantly reduced in 72 children with sickle cell disease compared with 40 age-matched black control children. There was significant correlation between functional activity of the total alternative pathway and functionally measured factor B, but not between factor B measured functionally and immunochemically. The opsonisation defect could be corrected in vitro by normal serum, and factor B-depleted serum, and was qualitatively similar to that seen in patients with primary yeast opsonisation deficiency. Serial studies showed that these serum defects were persistent. Reduction in the activity of components of the alternative pathway of complement and opsonisation was found in 4 patients who had recovered from pneumococcal meningitis and in one who developed osteomyelitis. Defects of yeast opsonisation and complement which are common in patients with sickle cell disease, may partly explain the children's increased susceptibility to infection, and might help to identify individuals especially at risk.

Adolescent↗
PubMed1984

Circulating immune complexes in regularly dialyzed patients with chronic renal failure.

The prevalence of circulating immune complexes (CIC) was investigated using the C1q binding assay (C1q BA) and the conglutinin binding assay (Kg BA) in 200 patients undergoing maintenance hemodialysis. Increased C1q binding was found in 45% (87 of 194) of the patients, and the modified Kg BA gave elevated values in 31% (20 of 65). The prevalence of CIC was similar in American and Swiss patients, and in patients undergoing hemodialysis, self-dialysis or peritoneal dialysis. In patients with 'nonimmunological' renal diseases, CIC were detected with similar frequency. No change in CIC was noted during hemodialysis in 6 additional patients tested. The abnormality was not related to age, sex, duration of dialysis, hepatitis B antigenemia, bacterial infections, or transfusions. Anti-DNA antibodies were absent in all subjects tested and the results of the C1q BA were not changed by DNase digestion of eight sera with high C1q binding. Rheumatoid factor activity (RF) was detected in approximately one-fifth of the patients, and there was a direct correlation between positive C1q binding and RF. There was no correlation between CIC and lymphocytotoxic antibodies. This study demonstrated a high prevalence of CIC in dialyzed uremic patients and established its relationship to other immunological abnormalities.

Antibodies, Antinuclear↗
PubMed1983

Complement components, C1 activation and disease activity in SLE.

Laboratory parameters were studied in 8 systemic lupus erythematosus patients during periods of high and low disease activity, mainly as defined by clinical criteria. Renal manifestations were present in 6 patients 5 of which showed antibodies to native DNA. C-reactive protein was raised in 3 patients. Only 1 of these showed a superimposed bacterial infection. Markedly high concentrations of C1r-C1s-C1 inactivator cOmplexes (C1r-C1s-Cl IA) in the sera provided direct evidence of C1 activation independent of disease activity. During active disease. C1r-C1s-C1 IA were correlated with C1q binding immune complexes as measured by solid phase, but not by fluid phase assay. Immunochemical concentrations of C1q, C4 and C3 and functional C2 were decreased in active SLE, consistent with sequential activation of the classical pathway. Discrepancies were noted between functional and immunochemical assay for C2 but not for factor B. Although essentially within the normal range, the levels of C1s, C4 binding protein, C5 and properdin were lower during active than during inactive disease. The concentrations of the factors B, I and H did not suggest involvement of the alternative pathway. 1 exceptional patient showed low factor B, a relative decrease of factor I and the presence of Bb fragments in plasma during active SLE. Markedly high factor D values were found. This could partly be explained by reduced renal function.

Adolescent↗
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↗
PubMed1985

Analytic study of the differential anticomplementary effects of dextran sulphate and heparin in the assay for the mouse alternative pathway.

In a recent paper, a linkage between immunological adjuvant activity in mice and in vitro anticomplementary (alternative pathway assay) effects was described for different polyanions. This connection was found only if mouse serum was used as a complement (C) source. In order to investigate the possible role of C in adjuvant activity, the differential effects of polyanions on mouse C were studied in detail. For this study, substances with different activity were selected, namely dextran sulphate with strong C-regulatory and immunoadjuvant activities, and heparin, which was weakly anticomplementary and devoid of adjuvant effect. In general, studies of mouse C are complicated by the unavailability of isolation procedures for the C-components involved. This difficulty was circumvented by making use of C5-deficient serum and of the haemolytic activity of mouse membrane attack complexes formed in the fluid phase. With yeast cells as alternative pathway activators it was shown that the effect of heparin on this pathway was restricted to activation of the terminal route. In contrast, dextran sulphate also caused a functional decay of a yeast-bound alternative pathway C5-convertase and interfered with the haemolytic activity of fluid-phase membrane attack complexes as well. Further studies will be needed to decide whether these specific effects of dextran sulphate are related to the immunological adjuvant activity of the substance in mice.

Animals↗
PubMed1986

C1 activation, with C1q in excess of functional C1 in synovial fluid from patients with rheumatoid arthritis.

Free Clq, in functionally active form was present in increased amounts in the synovial fluid of patients with rheumatoid arthritis. The presence of free Clq was associated with low concentrations of hemolytic C1, low C4 and raised amounts of C3dg/d fragments in the synovial fluid. The findings suggested intra-articular C1 activation with dissociation of C1 into free C1q and complexes containing C1r, C1s, and C1 inactivator. However, the immunochemical properties of synovial fluid C1r-C1s-C1 inactivator complexes appeared to differ from those of the complexes formed in serum, which hampered quantification with the assay used. Control patients with osteoarthritis or spondylarthritic syndromes did not show evidence of intra-articular complement activation, even though 1 patient with Reiter's disease had unexplained low concentrations of synovial fluid C4 and C3. The concentrations of circulating complement components were largely normal in the patients. Slightly increased concentrations of free C1q and C1r-C1s-C1 inactivator complexes in serum and C3dg/d fragments in EDTA plasma were observed, particularly in the patients with rheumatoid arthritis.

Adult↗
PubMed1982

Characterization of various immunoglobulin preparations for intravenous application. II. Complement activation and binding to staphylococcus protein A.

14 immunoglobulin preparations for intravenous use were tested to assess functions of their Fc portion. Inhibition of the hemolytic activity of complement, C1q binding and the interaction of IgG subclasses with Staphylococcus protein A were investigated. Complement studies were done on both the ready-for-infusion and the heat-aggregated preparations. Three groups of products could be distinguished: (1) Enzymatically and chemically treated products were devoid of complement-activating capacity, both when tested and ready-for-infusion and as heat-aggregated preparations. The chemically treated preparations showed atypical binding properties to Staphylococcal protein A. (2) The poly-(ethylene glycol) (PEG)-treated preparations and the untreated reference activated complement before and after heat-aggregation. (3) The albumin protected and the pH 4-treated product did not spontaneously activate complement in the ready-for-infusion state but did so after heat-aggregation. These results suggest that only the albumin-protected and the pH 4-treated products can be expected both to be well tolerated when given intravenously to high-risk agammaglobulinemic patients and to exhibit normal Fc functions in vivo.

Complement Activating Enzymes↗
PubMed1989

Monoclonal antibodies against components of the classical pathway of complement.

Activation of the classical pathway of complement involves several binding and enzymatic cleavage processes. Binding and enzymatic activation results in the appearance of new structures in the individual components. This report describes the different activation steps for C1q, C1r, C1s, C4 and C2 and summarizes monoclonal antibodies reported so far which recognize either conserved epitopes or activation-dependent epitopes with particular emphasis on neoepitopes occurring during the activation cascade.

Antibodies, Monoclonal↗