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PubMed1980

Interallelic competition and complementation in the ABO blood group system.

By means of quantitative agglutination, the results of interactions of A subgroup and variant genes with the B gene, as well as interactions of the Bx allele with A1, A2 and O genes in their heterozygous combination, are demonstrated. In the majority of interactions, competition occurs according to the rule that the allele producing the more active enzyme reduces the original activity of the enzyme produced by the relatively weaker allele. That the opposite result of interaction can occur also is shown in examples of Bx variants, when in A1Bx and A2Bx combinations complementation and a partial or nearly total normalization of the phenotypic expression of B antigen on red cells and in saliva happen. The phenomenon of competition, but even more so, the phenomenon of complementation, may have a broader importance than only for the ABO blood group system.

ABO Blood-Group System↗
PubMed2004

Genomic determination of CR1 CD35 density polymorphism on erythrocytes of patients with gallbladder carcinoma.

AIM: To study the changes of quantitative expression, adhering activity and genomic density polymorphism of complement types in erythrocytes (CR1) of patients with gallbladder carcinoma and the related clinical significance. METHODS: Polymerase chain reaction (PCR), Hind III restriction enzyme digestion, quantitative assay of CR1 and adhering activity assay of CR1 in erythrocytes were used. RESULTS: The number and adhering activity of CR1 in patients with gallbladder carcinoma (0.738+/-0.23, 45.9+/-5.7) were significantly lower than those in chronic cholecystitis and cholecystolithiasis (1.078+/-0.21, 55.1+/-5.9) and healthy controls (1.252+/-0.31, 64.2+/-7.4) (P<0.01). The number and adhering activity of CR1 in patients with chronic cholecystitis and cholecystolithiasis (1.078+/-0.21, 55.1+/-5.9) were significantly lower than those in healthy controls (1.252+/-0.31, 64.2+/-7.4) (P<0.05). There was a positive correlation between quantitative expression and adhering activity of CR1 (r = 0.79, P<0.01). Compared with those on preoperative day (0.738+/-0.23, 45.4+/-4.9), the number and adhering activity of CR1 in patients with gallbladder carcinoma decreased greatly on the third postoperative day (0.310+/-0.25, 31.8+/-5.1) (P<0.01), and on the first postoperative week (0.480+/-0.25, 38.9+/-5.2) (P<0.01), but they were increased slightly than those on the preoperative day (P>0.05). The number and adhering activity of CR1 recovered in the second postoperative week(0.740+/-0.24, 46.8+/-5.9) (P<0.01) and increased greatly in the third postoperative week (0.858+/-0.35, 52.7+/-5.8) (P<0.01) in comparison with those on the preoperative day and in the first postoperative week. The number and adhering activity of CR1 of gallbladder carcinoma patients with infiltrating, adjacent lymphogenous and distant organ metastases were significantly lower than those of gallbladder carcinoma patients without them (P<0.01). No difference was observed between the patients with gallbladder carcinoma and healthy individuals in the spot mutation rate of CR1 density gene (chi(2) = 0.521, P>0.05). The distribution of expression was 67.8% in high expression genomic type, 24.8% in moderate expression genomic type, and 7.4% in low expression genomic type. The number and adhering activity of CR1 high expression genomic type gallbladder carcinomas (0.749+/-0.22, 42.1+/-6.2) were significantly lower than those of healthy individuals (1.240+/-0.29, 63.9+/-7.2), and were also significantly lower than those of healthy individuals (0.921+/-0.23, 54.8+/-7.1), but no difference was observed between the number and adhering activity of CR1 lower expression genomic type gallbladder carcinomas (0.582+/-0.18, 44.3+/-5.5) and those of healthy individuals (0.610+/-0.20, 45.8+/-5.7) (P>0.05). CONCLUSION: Defective expression of CR1 in gallbladder carcinoma is mostly acquired through central peripheral mechanisms. The changes in CR1 quantitative expression and adhering activity are consanguineously related to the development and metastasis in gallbladder carcinoma.

Adult↗
PubMed1981

Role of cell-generated hydrogen peroxide in granulocyte-mediated killing of schistosomula of Schistosoma mansoni in vitro.

Human as well as murine granulocytes have been shown to kill the larval stages of helminth parasites; the mechanism of this cell-mediated cytotoxicity is, however, poorly understood. The present study was designed to assess the role of peroxidative processes in killing of schistosomula of Schistosoma mansoni by human granulocytes in vitro. The rate of H(2)O(2) production by human neutrophils, eosinophils, and basophils was measured upon incubation with schistosomula alone or in the presence of specific antibody or complement. Opsonized parasites (antibody and/or complement) increased the rate of H(2)O(2) production by neutrophils, eosinophils, and basophils by respective percentages of 500, 500, and 371. The rate of H(2)O(2) release was directly related to the number of granulocytes and to the proportion of cells attached to the surface of the schistosomula. Increased hydrogen peroxide release occurred by 10 min of incubation and was demonstrable up to 16 h after addition of leukocytes to schistosomula. The primary source of this oxygen product was found to be the granulocytes adherent to the schistosomula and not those that remained unattached. Hydrogen peroxide production by neutrophils and eosinophils was quantitatively similar (schistosomula coated with antibody plus complement stimulated 5 x 10(6) neutrophils and eosinophils to release H(2)O(2) at respective rates of 0.35 and 0.40 nmol/min). Granulocyte-mediated parasite killing correlated with rate of H(2)O(2) generation; both processes were inhibited by catalase. To define further the role of oxidative metabolites, neutrophils and eosinophils of two subjects with chronic granulomatous disease were used; marked reduction of granulocyte-mediated parasite mortality was observed. Peroxidase was required for H(2)O(2)-mediated killing. Addition of the peroxidase inhibitors azide (1 mM), cyanide (1 mM), or aminotriazole (1 cM) to neutrophilschistosomula mixtures significantly reduced parasite cytotoxicity (P < 0.01); similar reduction was observed when eosinophils were used (P < 0.01). Fixation of halide (iodide) to trichloroacetic acid-precipitable protein (2.4-6.0 nmol/h per 10(7) neutrophils) was demonstrated in the presence of granulocytes, opsonins, and parasites; this process was completely inhibited by 1 mM azide. These data indicate that contact between the surfaces of human granulocytes and schistosomula results in release of cellular hydrogen peroxide and iodination. The generation of H(2)O(2) and its interaction with peroxidase appear to be crucial in effecting in vitro granulocyte-mediated parasite cytotoxicity.

Animals↗
PubMed1980

In vitro effects of radiographic contrast media on the complement system.

The effect of several radiographic contrast media on the complement system in vitro was examined using quantitative crossed immunoelectrophoresis. Diatrizoate, iothalamate, metrizoate, and methiodal did not cause electrophoretic conversion of C3 or properdin factor B. In fact, the small degree of spontaneous conversion occurring when serum is incubated in polypropylene tubes was inhibited by these contrast media or by hypertonic sodium chloride. Metrizamide caused enhanced conversion of C3 and factor B that was only partially inhibited by ethylene glycol tetracetic acid (EGTA) but completely inhibited by ethylenediaminetetraacetic acid (EDTA). Iodipamide caused a unique electrophoretic alteration of C3 that was not affected by EDTA or several other inhibitors and that was not identical with the usual products of C3 activation. Iodipamide in very low concentrations inhibited complement activation through the classical pathway.

Citrates↗
PubMed1961

The interaction of mammalian cells with antibodies. I.

The single cell plating technique has been applied to quantitation of the reproductive killing of mammalian cells by specific antibodies. This method confirms previous demonstrations by other workers of localization of all the killing activity in the gamma-globulin fraction of specific cell antisera but not of normal sera; the need for complement for the killing action in low doses of antibody and the leakage of cell constituents attending cell killing under these conditions. In concentrations of 4 per cent or higher of heated antiserum cell killing occurs without added complement. The cell plating technique permits highly reproducible quantitation of antibody action and demonstrates antibody activity in sera diluted 1:3000. It permits demonstration of very high degrees of species specificity as shown by virtually complete absence of cross-reaction between antisera to Chinese hamster and S3 HeLa cells, respectively. Somatic cells which have been sensitized by absorption of specific antibody lose their sensitization when incubated at 37 degrees unless complement is added within 1 hour.

Animals↗
PubMed1976

[Multiple sclerosis with reduced and with normal levels of complement in the blood. Clinical and genetic correlation].

The authors describe the results of immunological assay of complement factors C3, C4 (the usual path of activation of complement) and of B factor (the alternate path of activation) in 61 multiple sclerosis patients not receiving corticoids, 52 normal controls and 217 patients with other neurological disorders. Hypocomplementaemia (fall in factor C3 related to a fall in total haemolytic activity) was found in 29.5 p. 100 of the patients not on corticotherapy at the first assay, and in 36 p. 100 of the patients when repeated assays were carried out. Hypocomplementaemia is significantly more frequent in multiple sclerosis than in the normal population (0 p. 100) and in neurological patients (9.6 p. 100). In 13.1 p. 100 of the multiple sclerosis patients there was a decrease in B factor: 50.3 p. 100 of the multiple sclerosis patients exhibited no quantitative abnormality of the main factors of complement (normocomplementary multiple sclerosis). The group of multiple sclerosis patients with hypocomplementaemia was characterized by the incidence of other abnormalities in the complement system: cleavage of the C3 factor and a fall in B factor in 60 p. 100 of the cases. A more frequent increase in IgE and measles antibodies was found also while the normocomplementary multiple sclerosis patients more frequently had higher levels of IgA. Genetically, the group with hypocomplementaemia is related to a significant increase in the incidence of the HL-A W18 group while the normocomplementary multiple sclerosis patients appear closely related to the HL-A7 group. Familial investigations show that hypocomplementaemia is usually present in the ascendents and collaterals and that it seems to be transmitted with the HL-A haplotypes. Four families gave evidence of transmission with the W18 group. This transmission sometimes occurs together with transmission of an increase in IgE and/or of measles antibodies. In two pedigrees, one of the ascendents carried in his serum an activator of the alternate path of complement. There does not appear to be any prognostic difference between the two groups. In multiple sclerosis with hypocomplementaemia, the facts suggest a complex immunological abnormality, transmitted genetically to the subject and existing prior to the illness, comprising both elements of deficient and excessive immune response. The recognized presence of a gene of immunological reactivity and of genes of synthesis of complement on the 6th chromosome, in proximity with genes of histocompatability (HL-A and M.L.C.) provides a theoretical basis for this supposition.

Adult↗
PubMed1988

Binding and activation of C4 and C3 on the red cell surface by non-complement enzymes.

We investigated the binding of C4 and C3 to red cell surfaces by non-complement enzymes. Cell bound C components were quantitated by a radioimmunoassay, the chain structure of bound components was analyzed by Western blotting and the hemolytic activity of bound components was determined. Trypsin, chymotrypsin, plasmin, elastase, thrombin, kallikrein and enzymes from Bacillus subtilis, Staphylococcus aureus and Streptomyces griseus all were found capable of binding C4b and C3b to sheep red cells. C4b bound by any of these enzymes was hemolytically active; both classical and alternate pathway activity of C3 could be demonstrated for most enzymes except plasmin and thrombin. In addition, trypsin and the bacterial enzymes were also able to generate the classical pathway C3-convertase from C4b + C2. The hemolytic efficiency of enzyme bound C4b and C3b was about the same as for these molecules bound by complement enzymes. In contrast, the process of binding by the non-complement enzymes was several hundred-fold less efficient than by cell bound complement enzymes. The results demonstrate that several enzymes can replace the C1 and C42 enzymes in the classical pathway and are able to initiate the alternative pathway by activating C3 and binding C3b to the cell surface.

Animals↗
PubMed1993

Two-site ELISA for quantification of the terminal C5b-9 complement complex in plasma. Use of monoclonal and polyclonal antibodies against a neoantigen of the complex.

A quantitative ELISA procedure using monoclonal and polyclonal antibodies against neoantigens of the terminal C5b-9 complement complex has been developed. The ELISA was demonstrated to be both sensitive and reproducible. The normal range for C5b-9 determinations, defined as 2.5-97.5% interval of the values obtained in 76 healthy blood donors, was 3.12-10.3 AU/ml. The presence of rheumatoid factor did not affect the determination of C5b-9 as demonstrated by immunoabsorption studies.

Antibodies, Monoclonal↗
PubMed2004

Methods for genetic dissection of complex traits.

In this Perspective, the author responds to a recent SAGE KE Perspective. An alternative view of the benefits of quantitative trait loci mapping as a way to understand the molecular mechanisms of life-span determination is presented.

Animals↗
PubMed2000

The application of human complement factor H-related protein (BTA TRAK) in monitoring patients with bladder cancer.

The BTA TRAK assay is a quantitative sandwich format enzyme immunoassay performed in a reference laboratory. It measures levels of human complement factor H-related protein (hCFHrp) which is similar to human complement factor H. Test characteristics reveal an overall sensitivity of 68% to 77.5% and a specificity of 50%-75%. Retrospective analysis of urine specimens employing hazard analysis suggests that BTA TRAK may have a role as a quantitative diagnostic marker in monitoring bladder cancer patients. Prospective studies are required to validate this application and other uses of the BTA TRAK assay in the management of bladder cancer patients.

Antigens, Neoplasm↗
PubMed1998

Platelet adhesion, contact phase coagulation activation, and C5a generation of polyethylene glycol acid-grafted high flux cellulosic membrane with varieties of grafting amounts.

Grafting of polyethylene glycol chains onto cellulosic membrane can be expected to reduce the interaction between blood (plasma protein and cells) and the membrane surface. Alkylether carboxylic acid (PEG acid) grafted high flux cellulosic membranes for hemodialysis, in which the polyethylene glycol chain bears an alkyl group at one side and a carboxyl group at the other side, have been developed and evaluated. PEG acid-grafted high flux cellulosic membranes with various grafting amounts have been compared with respect to platelet adhesion, the contact phase of blood coagulation, and complement activation in vitro. A new method of quantitating platelet adhesion on hollow-fiber membrane surfaces has been developed, which is based on the determination of lactate dehydrogenase (LDH) activity after lysis of the adhered platelets. PEG acid-grafted high flux cellulosic membranes showed reduced platelet adhesion and complement activation effects in grafting amounts of 200 ppm or higher without detecting adverse effects up to grafting amounts of 850 ppm. The platelet adhesion of a PEG acid-grafted cellulosic membrane depends on both the flux and grafting amounts of the membrane. It is concluded that the grafting of PEG acid onto a cellulosic membrane improves its biocompatibility as evaluated in terms of platelet adhesion, complement activation, and thrombogenicity.

Animals↗
PubMed1986

Serological diagnosis of influenza A infections in the horse by enzyme immunoassay. Comparison with the complement fixation test.

An enzyme immunoassay (EIA) using horseradish peroxidase and a type-specific antigen is described for the detection and quantitation of anti-influenza antibodies in the horse. Compared with the complement fixation (CF) test (using the same antigen), EIA proved to be superior with respect to sensitivity and reliability. The internal variation of EIA was low and thus small titres in EIA can be considered of diagnostic significance. However, no strict correlation with CF was observed. The use of an immunoconjugate against equine IgM in parallel with IgG would certainly improve the sensitivity of the test, especially in early stages of infection.

Animals↗
PubMed1982

Tumor promoter 12-O-tetradecanoylphorbol 13-acetate: effect on complement and Epstein-Barr virus receptors in human lymphoblastoid cell lines.

The effect of the tumor promoter 12-O-tetradecanoylphorbol 13-acetate (TPA) on the C3 and Epstein-Barr virus (EBV) receptors in various human lymphoblastoid cells was investigated with the use of the erythrocyte-antibody-complement (EAC) rosette formation method and a quantitative bioassay for EBV receptors. TPA caused a significant decrease of C3 receptors in the cultures of both Raji and SB4 cells (by approximately 50% of the C3 receptors in untreated cultures at 10 ng/ml). Kinetic studies revealed that the rate of reduction was rather moderate but progressive, reaching a maximum 5 days after treatment with TPA. Kinetic studies showed that EBV receptors also decreased, similar to the reduction seen with C3 receptors after TPA treatment. The effect of TPA on the reduction of C3 receptors was observed not only in these cells but also in other EBV-positive B-cells, subclones of SB4 cells, and MOLT-4 cells. However, in an EBV-negative B-cell line, BJAB, EAC rosette formation was significantly enhanced.

Burkitt Lymphoma↗
PubMed1999

Differential complement activation by bovine IgG2 allotypes.

Immunoglobulin allotypes and complement (C) are known to be related to susceptibility to infection. Because bovine IgG2 is important in resistance to pyogenic infections and because its two allotypes, IgG2a and IgG2b, differ in sequence in the CH1, hinge, CH2, and CH3 regions, we tested the ability of these allotypes to initiate the bovine C cascade. Bovine IgG2a and IgG2b were standardized according to specific anti guinea pig red blood cell (GPRBC) ELISA activity using anti IgG2 reagents shown essentially unbiased for allotype. Complement activating activity of the allotypes was quantitated in a GPRBC lysis assay. With this system, IgG2b consistently had more than twice the activity in bovine C mediated lysis as compared with IgG2a. The fact that both EDTA and EGTA/Mg almost completely inhibited C mediated lysis of GPRBCs indicated that lysis was due to the classical pathway. Since antibody usually activates C by the classical pathway, this supports the supposition that activation was by the IgG2-GPRBC complexes. Flexibility analyses showed that IgG2b had a more rigid hinge than IgG2a, perhaps partially explaining the greater efficiency of IgG2b in C activation. Other mechanisms may include differences in glycosylation and in the amino acid at position 332. The difference in ability to activate C may mean that animals of the IgG2a allotype could be more susceptible to infection with extracellular pyogenic pathogens which are killed by C or by phagocytes after opsonization with IgG2 and C.

Animals↗
PubMed1976

Inconsistency of the tibia test for estimating growth hormone in crude pituitary extracts.

The complement fixation immunoassay (CFIA) was used for quantitating growth hormone (GH) in crude anterior pituitary extracts from rats subjected to thyroidectomy with or without cortisol and exogenous GH administration. The results obtained from this study were compared with pertinent bioassay (tibia test) results or correlated with the pituitary acidophil cell counts. Whereas it has been reported that pituitary GH levels are normal by the tibia test at 2 weeks after thyroidectomy, the highly specific CFIA method showed an actual 87% decrement which correlated well with the reduction in acidophilis. In addition, the apparently normal content of GH after cortisol administration to thyroidectomized rats, as measured by the tibia test, was contradictory to the very low acidophil population and to the marked reduction in pituitary GH content as measured by the CFIA. Furthermore, theoretical tibia responses illustrate the inconsistency of the bioassay in different experimental conditions. If, as previously suggested, the content of thyrotrophin (TSH) in the crude pituitary extracts renders the bioassay of GH a dubious procedure, then the superiority of immunoassay is obvious.

Animals↗
PubMed1994

Human immunodeficiency viruses regulated by alternative trans-activators: genetic evidence for a novel non-transcriptional function of Tat in virion infectivity.

Thirteen genetically altered HIV-1 proviruses were created. These various genomes can be segregated into three groups: (i) a set of tat(-) viruses that have a functional HTLV-I Tax inserted in nef; (ii) a set of tat(-) viruses with Gal4 binding sites inserted in U3 and a Gal4-VP16 cDNA inserted in nef; and (iii) a set of tat(+) HIV genomes that are 5' and 3' TAR(-) and are Gal4-binding-site(+) in U3 and Gal4-VP16(+) in nef. We found that viruses in groups (i) and (ii), although tat(-), were fully complemented for viral gene expression based on quantitative measurements of viral protein synthesis and on the visualization by electron microscopy of the proper assembly of morphologically correct virions. Interestingly, group (i) and (ii) virions were defective in a spreading cytopathic infection when assayed in T-lymphocytes. Group (iii) viruses, although capable of producing intact Tat protein, also could not use Tat for transcription/gene expression because of the TAR(-) genotype. However, this class of viral genomes produced viruses that were highly infectious and cytopathic in primary and in continuously propagated T-lymphocytes. These three groups of viruses are all transcriptionally Tat-TAR independent. Their distinct differences in infectivity/cytopathicity provide genetic evidence that Tat provides a transcriptionally independent function in determining infectivity and cytopathicity in the setting of a spreading viral infection. Given that all HIV virions normally contain four intact copies of TAR RNA, our findings suggest a re-examination of whether Tat could be a virion-TAR-associated protein and the possible implications of this for virus infectivity/cytopathicity.

Base Sequence↗
PubMed1992

Fibroblast-dependent tumorigenicity of melanoma xenografts in athymic mice.

Two human melanoma cell lines, UCT-Mel 2 and UCT-Mel 3, were invariably tumorigenic in nude mice when inoculated s.c. in doses of 10(6) cells or higher; 10(5) cells or less did not give rise to tumours. In this report we show that otherwise sub-tumorigenic inocula developed into vigorously growing tumour xenografts when co-inoculated with normal fibroblasts. Fibroblasts derived from adult, neonatal or embryonic tissues all functioned as complementing cells, as did cells of human or murine origin. There was, however, a requirement for complementing cell viability, since ethanol-killed fibroblasts were inefficacious. The fibroblast effect was dose-dependent and was not observed if injections of fibroblasts and melanoma cells were separated anatomically or temporally. We have shown, by titrating admixtures of melanoma cells and fibroblasts, that fibroblasts are, in quantitative terms, more efficacious than melanoma cells as complementing cells. The system we describe provides a useful model for the study of stromal-cell regulation of tumour growth.

Animals↗