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PubMed1979

Serum complement concentrations, nutritional status and the outcome of measles and measles pneumonia.

A prospective study of children with measles has shown a significant association between malnutrition and a poor prognosis. Levels of a number of complement components bore no relationship to the severity of the disease or to its prognosis. Some of the children with acute measles had depressed serum concentrations of factor D, Clq or C3, but complement deficiency does not appear to be implicated in the heightened susceptibility to secondary bacterial and viral infection so commonly found after acute measles.

Body Weight↗
PubMed1978

The structural events associated with the attachment of complement components to cell membranes in reactive lysis.

Electron microscopic study of the events occurring at the cell membrane during reactive lysis by complement, showed that a foliaceous particle was formed at the C5b-7 stage, that enlarged to a particle with a variable number of arms at the C5b-8 stage. Up to this point, no typical complement lesions were found. At the C5b-9 stages, the particles were completely converted to typical complement lesions, i.e. hollow cylinders projecting from the cell membrane and partly penetrating it. C5b-9 complexes assembled in the fluid phase did not show the typical structure of the lesions, but were amorphous masses of fibres.

Complement C5↗
PubMed1991

C3 activation products, C3 containing immune complexes, the terminal complement complex and native C9 in patients with rheumatoid arthritis.

Complement activation products, C9 and C3-containing circulating immune complexes (CIC), were evaluated in plasma and synovial fluid (SF) from patients with rheumatoid arthritis (RA) and osteoarthritis. C3 activation products and the fluid phase terminal complement complex were considerably elevated in SF from RA patients reaching levels five- to eighttimes that in plasma, consistant with a local activation of the whole cascade in the joints. The results emphazise the importance of detecting C3 activation by neoepitope expression instead of single fragment determinations. The concentration of native C9 was lower in synovial fluid compared with plasma, consistant with the excessive local complement activation. Increased CIC levels which correlated with the degree of complement activation were also found in the SF from the RA patients.

Adult↗
PubMedDate not supplied

The occurrence of precipitating antibodies in transfused Japanese patients with hereditary ninth component of complement deficiency and frequency of C9 deficiency.

Antibodies to the ninth component of complement (C9) were found in a patient with hereditary C9 deficiency (C9D) who had received multiple transfusions. The incidence of anti-C9 precipitating antibodies following transfusion was investigated in 63,625 patients treated at Kyushu University Hospital, and 475,886 blood donors at the Fukuoka Red Cross Blood Center were studied to determine the frequency of C9D in Japan. Transfusion reactions in recipients having anti-C9 were also monitored. One hundred and eighty-six subjects (15 patients and 171 donors) with C9D were identified (a prevalence of 0.036%). Four of 15 C9-deficient patients had received transfusions. One of the patients who had received several units of blood within 1 week developed low-titer C9-precipitating antibody. This patient was transfused in the presence of the antibody without evidence of adverse reactions. No precipitating antibody was detected in the remaining three patients who had received several units of blood on a single day. These observations suggest that multiple transfusions may contribute to the development of anti-C9.

Chemical Precipitation↗
PubMed1990

Paroxysmal nocturnal haemoglobinuria with coexisting deficiency of the ninth component of complement: lack of massive haemolytic attack.

A 47-year-old woman with paroxysmal nocturnal haemoglobinuria (PNH) was found to have an inherited deficiency in the ninth complement component (C9). In complement-sensitivity lysis tests, 80% of her erythrocytes were markedly complement-sensitive (PNH-III). Laser cytofluorimetry with a monoclonal antibody against decay-accelerating factor (DAF) revealed that 95% of her erythrocytes were DAF-negative. Surprisingly, she has suffered only mild haemolysis and has never experienced massive spontaneous haemolysis. Gross haemoglobinuria and jaundice occurred only after receiving postoperative transfusion of whole blood. In her serum, C9 was not detectable either by immunological or by functional assays. Both the Ham test and the sugar water test using normal human serum or plasma yielded marked haemolysis of the patient's erythrocytes. When the patient's serum or plasma was used, only a trace of lysis was detected. Addition of purified human C9 to her plasma fully restored haemolysis. These observations indicated that C9 may play a critical role in haemolytic attacks in patients with PNH and that characteristic haemolysis in PNH may be tempered by coexisting C9 deficiency.

Complement C9↗
PubMed1986

Increased hemolytic activity of the trypsin-cleaved ninth component of complement.

Human C9 treated with trypsin is initially cleaved into two fragments with relative mol. wts of 53,000 and 20,000. This limited cleavage of C9 induces a 2.4-times increase in the hemolytic activity of C9 when compared to untreated C9. This difference diminishes when C9 activity is tested in an assay using a prolonged incubation time of C9 with C5b-8-bearing red blood cells. Trypsinization of C9 also promotes spontaneous C9 polymerization. SDS-resistant tubular C9 complexes are formed at a C9 concn of 1 mg/ml within 8 hr at 37 degrees C. Our data indicate that specific limited proteolysis of C9 not only induces spontaneous C9 polymerization but also increases the hemolytic activity of C9, suggesting that a similar molecular mechanism is involved in both processes.

Biopolymers↗
PubMed1985

The LDL receptor gene: a mosaic of exons shared with different proteins.

The multifunctional nature of coated pit receptors predicts that these proteins will contain multiple domains. To establish the genetic basis for these domains (LDL) receptor. This gene is more than 45 kilobases in length and contains 18 exons, most of which correlate with functional domains previously defined at the protein level. Thirteen of the 18 exons encode protein sequences that are homologous to sequences in other proteins: five of these exons encode a sequence similar to one in the C9 component of complement; three exons encode a sequence similar to a repeat sequence in the precursor for epidermal growth factor (EGF) and in three proteins of the blood clotting system (factor IX, factor X, and protein C); and five other exons encode nonrepeated sequences that are shared only with the EGF precursor. The LDL receptor appears to be a mosaic protein built up of exons shared with different proteins, and it therefore belongs to several supergene families.

Amino Acid Sequence↗
PubMed1989

Inherited deficiencies of the late-acting complement components other than C9 found among healthy blood donors.

Among sera from 145,640 healthy blood donors in Osaka, 16 were found to have abnormalities in late-acting complement components other than C9. It was found that of these 16 sera, 2 were deficient in C5, 4 in C6, 6 in C7 and 4 in C8 alpha-gamma-subunit. The incidence of deficiency of each component among the Osaka blood donors was calculated as follows: C5 deficiency, 0.0014%; C6 deficiency, 0.0027%; C7 deficiency, 0.0041%; C8 alpha-gamma-subunit deficiency, 0.0027%. We confirmed that 13 donors were healthy and 12 had no past history related to a complement component deficiency. From these results, not only C9 deficiency but also deficiencies of the other late-acting complement components were found among the healthy blood donors, but no early-acting component deficiencies were noted.

Blood Donors↗
PubMed1987

Induction of synthesis of the cytolytic C9 (ninth component of complement)-related protein in human peripheral mononuclear cells by monoclonal antibody OKT3 or interleukin 2: correlation with cytotoxicity and lymphocyte phenotype.

Synthesis of the cytolytic C9-related protein (C9RP) was induced by activation of resting human peripheral T lymphocytes with the anti-CD3 antibody OKT3 or interleukin 2. Comparison of cellular cytotoxicity and C9RP content at various times during activation yielded a coefficient of correlation r = 0.92. During OKT3 stimulation of peripheral mononuclear cells, maximal C9RP content and cytotoxicity were observed by day 2 or 3, with subsequent decline to baseline values by day 5, whereas during interleukin 2 stimulation, both parameters reached the maximal level at days 3-5. After fluorescence-activated cell sorting, C9RP and cytotoxicity were quantitated in CD4+, CD8+, and Leu-19+ subsets. In OKT3-activated CD8+ cells, C9RP increased to approximately 3 X 10(6) molecules per cell, with a corresponding increase in lysis of human melanoma cells mediated by anti-CD3-anti-melanoma monoclonal antibody conjugates. Interleukin 2-stimulated CD8+ cells showed similar increases, but cytotoxicity was conjugate-independent. Activated CD4+ cells showed minimal increase in C9RP content. Leu-19+ cells, which exhibit natural killer cell activity, had a high C9RP content (approximately 2.5 X 10(6) molecules per cell) before stimulation.

Antibodies, Monoclonal↗
PubMed1991

Ectocytosis caused by sublytic autologous complement attack on human neutrophils. The sorting of endogenous plasma-membrane proteins and lipids into shed vesicles.

During sublytic complement attack on human neutrophils, plasma-membrane vesicles are shed from the cell surface as a cell-protection mechanism. By using surface-iodinated neutrophils it was found that less than 2% of surface label was recovered in shed vesicles under conditions where 40% of complement component C9 was shed. SDS/PAGE of 125I-labelled shed vesicles and plasma membranes showed differences in iodination pattern, demonstrating the sorting of membrane proteins into the shed vesicles. Analysis of 32P-labelled phospholipids after labeling of neutrophils with [32P]Pi before sublytic complement attack showed the presence of phosphatidic acid, phosphatidylcholine, phosphatidyl-ethanolamine, phosphatidylinositol and polyphosphoinositides in shed vesicles. Quantitative analysis using [3H]acetic anhydride-labelling method showed that the molar proportions of phosphatidylethanolamine, phosphatidylinositol, phosphatidylserine and sphingomyelin were the same in shed vesicles as in plasma membranes. In contrast, the molar proportions of cholesterol and diacylglycerol relative to sphingomyelin were almost twice those found in plasma membranes. The data demonstrate the existence of protein and lipid sorting mechanisms during the formation of shed vesicles when neutrophils are subject to sublytic complement attack. The term 'ectocytosis' is proposed to describe triggered shedding of right-side-out membrane vesicles from the surface of eukaryotic cells.

Autoradiography↗
PubMed1992

Regulation of complement functional efficiency by histidine-rich glycoprotein.

The modulation of complement functional efficiency by serum histidine-rich glycoprotein (HRG) was investigated. Addition of exogenous HRG to prewarmed diluted serum, followed immediately by sensitized sheep erythrocytes (EA), resulted in enhanced hemolysis. However, when HRG was incubated with diluted serum for 10 minutes at 37 degrees C, inhibition of hemolysis occurred. The biphasic modulation of complement function was also obtained with the complement alternative pathway when HRG was added to diluted serum for hemolysis of rabbit erythrocytes. Partial reduction of complement functional activity was shown when serum was absorbed by an HRG-Sepharose 6MB column. Western blot analysis showed that complement C8, C9, factor D, and S-protein in diluted serum were bound by nylon membrane-immobilized HRG. However, by immunoprecipitation of relatively undiluted serum with anti-HRG IgG beads, HRG was found to coprecipitate with S-protein and plasminogen, which suggested that HRG may complex with these proteins in serum. In functional tests, HRG inhibited C8 hemolytic activity, probably by preventing C8 binding to EAC1-7 cells. HRG also enhanced polymerization of purified C9 as well as the generation of a 45-Kd C9 fragment. Such an effect was even more pronounced in the presence of divalent cations with the reaction mixtures of C9 and HRG. Partial dimerization of C9 was shown when exogenous HRG was added to normal serum. In contrast, polymerization of serum C9 was inhibited by exogenous HRG during poly I:C activation of serum or incubation under low ionic strength conditions. HRG was further shown to inhibit factor D-mediated cleavage of factor B when bound by cobra venom factor. The molecular basis by which HRG regulates serum complement function is not clear. Hypothetically, the tandem repetitions of a consensus histidine-rich penta-peptide sequence in HRG may provide a highly charged area that interacts with complement components.

Animals↗
PubMed1987

Double immunofluorescence studies of IgA and poly C9 (MAC) in glomeruli from patients with IgA nephropathy.

Double immunofluorescent studies on IgA, poly (MAC) or C3 in glomeruli from patients with IgA nephropathy are described. Renal biopsy specimens were obtained from 12 patients with IgA nephropathy, four patients with proliferative glomerulonephritis (PGN) and two normal human kidney (NHK). These specimens were incubated with monoclonal anti-poly C9 (membrane attack complex; MAC) and then stained with FITC-labelled goat anti-mouse immunoglobulin (Ig) antiserum. After washing with phosphate buffered saline (PBS) (pH 7.4), the sections were stained with rhodamine-labelled rabbit anti-human IgA antiserum and examined by fluorescence microscopy. The sections were also stained with FITC-labelled goat anti-human C3 antiserum and then stained with rhodamine-labelled rabbit anti-human IgA antiserum. Markedly combined depositions of IgA and poly C9 or C3 in glomeruli were observed in patients with IgA nephropathy. There was a significant correlation between the deposition of poly C9 and the grading of histopathological injuries in such patients. There was also a significant correlation between the deposition of poly C9 in the extraglomerular vascular vessels and the ageing in patients with IgA nephropathy, PGN and NHK. It appears that the deposition of poly C9 might detect directly the activities of complement in glomeruli from patients with IgA nephropathy.

Age Factors↗