Biomedical subjects

A Capron

Publications and source records attributed to A Capron.

At least 595 records · Page 33Linked to original sources

PubMed1980

Evaluation of circulating antigens by a sandwich radioimmunoassay, and of antibodies and immune complexes, in Schistosoma mansoni-infected African parturients and their newborn children.

Circulating Schistosoma mansoni soluble antigens (CSA), circulating anti-S. mansoni antibodies (CAb), and immune complexes (CIC) were studied in three groups of African patients living in the same area. The first two groups were composed of 26 S. mansoni-infected mothers and their 26 uninfected newborn children. The third group included 13 men and 10 non-pregnant women who were also infected with S. mansoni. CSA were quantified by using a solid phase sandwich radioimmunoassay, which was shown to be sensitive, reproducible, and S. mansoni-specific. CAb were studied by indirect hemagglutination. CIC evaluations were performed by using the Clq binding test. A high correlation was shown between the CSA levels in sera from infected mothers and from the umbilical cord of their newborn children, indicating that CSA are probably transferred through the placenta. CSA levels in mothers were significantly higher than in the third group, in which no difference was found between men and women. On the other hand, CAb and CIC were significantly higher in the third group than in the group of mothers, indicating that CSA levels may be modulated by the immune response of the host.

Adolescent↗

PubMed1980

Role of anaphylactic antibodies in immunity to schistosomes.

Antibody-dependent cell-mediated cytotoxicity in reinfection immunity to schistosomes in the rat involves either IgG2a anaphylactic antibody and eosinophils or IgE antibody and macrophages. The first system requires two signals, one by the antibody through the eosinophil Fc receptor, another by mast cells through the release of mediators among which is ECF-A. IgE antibody complexed with schistosome antigen binds to an IgE-specific receptor on the macrophage and triggers the cell to release enzymes and superoxide. Immunity in rat schistosomiasis is antibody-dependent, abolished in anti-mu treated neonate rats or by passive serum transfer after selective depletion of either IgG2a or IgE. The two anaphylactic antibody-dependent cell cytotoxicity systems are in a permanent balance in immune rats, eosinophils being blocked by IgG2a immune complexes when this cell is inefficient. Anaphylactic antibodies thus play a key role in triggering and modulating effector cell function.

Animals↗

PubMed1980

Enzyme release and superoxide anion production by human alveolar macrophages stimulated with immunoglobulin E.

Human alveolar macrophages specifically released lysosomal beta-glucuronidase and neutral proteases when successively incubated with IgE, and then, for 30 min, with anti-IgE. Superoxide anion O2- generation was obtained when anti-IgE-opsonized zymosan was added to IgE-incubated cells. Macrophages from smokers excreted twice as much enzymes and superoxide as cells from non-smokers. It was possible to induce the specific release of beta-glucuronidase with normal alveolar macrophages successively incubated with the serum of patients allergic to house dust or to grass pollen and then with the specific allergen. This characteristic opens the field to a direct test for allergic sera by analogy with the allergen-induced degranulation test of sensitized basophils.

Allergens↗

PubMed1980

Effect of neonatal injection of anti-mu antibodies on immunity to schistosomes (S. mansoni) in the rat.

The effect of neonatally initiated injections of anti-mu serum on immunity to reinfection with Schistosoma mansoni in the rat was investigated in vitro and in vivo. Anti-mu treatment resulting in a profound depression of immunoglobulin synthesis dramatically decreased immunity to reinfection assessed by worm recovery technique. Complement-dependent antibody, IgG2a antibody-eosinophil-mediated and IgE-macrophage cytotoxicity reactions were in parallel markedly reduced. These results show the prominent role played by antibody-dependent mechanisms in immunity to schistosomes in the rat.

Animals↗

PubMed1980

Purification, immunochemical, and biologic characterization of the Schistosoma circulating M antigen.

Circulating M antigen, specific for genus Schistosoma, was previously described in serum, urine, patients' milk, and in serum and urine of animals infected by S. mansoni. The M antigen was thermostable and soluble in trichloroacetic acid. It was not hydrolyzed by protease, ribonuclease, amylase, or neuraminidase but destroyed by sodium metaperiodate. In the present study, we have purified the M ag by using trichloroacetic acid solubility, DEAE Sephadex, and immunoadsorption. The M ag showed a neutral electric charge, a m.w. heterogeneity, and was only stained by periodic acid-Schiff. The composition study revealed M ag was a glycoprotein with a polysaccharide moiety (63% of the molecules) particularly rich in galactose, fucose, glucosamine, and mannose, and with a high molecular ratio of serine and threonine. The presence of O-glycosidic linkage allowed M ag to be considered as a mucin or a mucus glycoprotein-like component. It was localized in the cell wall of the gut of adult worms.

Amino Acids↗

PubMed1980

Interaction between Schistosoma mansoni and the complement system: binding of C1q to schistosomula.

In earlier studies we have found that activation of the classical complement pathway (CCP) by the immature schistosomes involves the presence of IgG. By investigating the first step of this activation we have demonstrated in the present work that binding of C1q to schistosomula can occur by two different routes: 1) directly, by specific C1q receptors, and 2) indirectly through the IgG previously attached to Fc receptors present on the parasite surface. Only this second mechanism appears to be involved in CCP activation by schistosomula. Moreover, certain low m.w. schistosome antigens (less than 20,000), which activate CCP, also directly fixed C1q. In this case, IgG are not required for C activation. The presence of receptors for host protein, essentially in 2- to 3-hr-old schistosomula, i.e., the life stage of Schistosoma mansoni that are first in contact with the host, could be the first mechanism by which the schistosomes evade the immune attack.

Animals↗

PubMed1980

Evaluation of the enzyme-linked immunosorbent assay (ELISA) and other serological tests for the diagnosis of toxoplasmosis.

The enzyme-linked immunosorbent assay (ELISA) was evaluated in human toxoplasmosis in three laboratories using their own procedures. The same batch of serum samples was investigated in the three laboratories. ELISA results were compared by statistical analysis both with one another and with those of the dye test (DT), immunofluorescence (IF), complement fixation test (CFT), and indirect haemagglutination (IHA).Highly significant correlations were obtained between the three laboratories with ELISA using two different antigens and enzyme conjugates. The correlations between ELISA and the other serological tests showed the following sequence: CFT>IF>IHA>DT. Highly significant correlations were obtained between ELISA using anti-gamma-chain and anti-total immunoglobulin conjugates. The agreement in discrimination between sera with low and high antibody levels was good for all the different ELISA techniques but discrimination between positive and negative sera depended rather on the ELISA procedure used.

Enzyme-Linked Immunosorbent Assay↗

PubMed1980

[Cellular interactions of IgE: towards a new function for IgE].

The anaphylactic function of IgE has been intensively investigated. The Fc epsilon receptor on mast cells or basophils combines with the last two constant domains of the epsilon heavy chain. The Fc epsilon receptor is apparently a glycoprotein, monovalent and free in the plasma membrane. The interaction between the antigen (allergen) and the corresponding IgE antibody combined with the Fc epsilon receptor results in the aggregation of the receptors. Receptor dimerization suffices to trigger the cell. Compartments can be described in mast cells or basophils, the activity of which depends upon the number of formed receptor dimers on the corresponding membrane area. Beyond a threshold number of dimerized receptors, the cell compartment is triggered, which in the presence of Ca++ leads to the discharge of mast cell mediators, an increasing function of the dimer number. Excess receptor aggregation or the absence of aggregation (i.e. IgE-Ag2 complexes) deactivates the cell, which occurs more often in the absence of Ca++. Thus, IgE molecules play a passive role only in allowing the aggregation of the receptors which delivers the activating signal. But through the composition of IgE-antigen complexes bound to the receptors, IgE also modulates the cell function according two antagonistic reactions in permanent balance, i.e. activation or deactivation. IgE molecules are also involved in immediate type reactions in inducing the release of lysosomal enzymes from mononuclear phagocytes. But IgE antibody can also, when complexed with the antigen, trigger macrophage cytotoxicity for the corresponding target, which indicates a new function of IgE in the effector mechanisms of immunity of particular importance in immunity to schistosomes. A receptor for aggregated IgE has been characterized on the membrane of macrophages. The binding of IgE to its macrophage receptor triggers the cell, as shown by the resulting increase in cyclic GMP, calcium uptake and accelerated turn-over of lysosomal enzymes. A receptor for IgE has also been described on lymphoid cells, B cells, null cells and recently T cells, and the appearance of the receptor is modulated by IgE molecules themselves, suggesting a homeostatic role of IgE molecules. IgE appears thus to play various functions, the most dramatic being the triggering of anaphylactic reactions. But the role of IgE in activating mononuclear phagocytes or lymphoid cells might also prove to be of importance in immunity.

Animals↗

PubMed1980

IgE antibody-mediated cytotoxicity of rat macrophages against microfilaria of Dipetalonema citeae in vitro.

The Fischer rat develops an acquired resistance against circulating microfilariae. Macrophages from the peritoneal washings of normal rats preincubated at 37 degrees C with the sera obtained from rats immune to circulating microfilariae adhered to and kill the microfilaria of Dipetalonema viteae in vitro within 16 to 24 hr. No significant adherence and cytotoxicity was mediated by sera collected from animals with microfilaraemia or from normal rats. Adherence of macrophages to microfilaria was associated with damage to the surface of the larva as revealed by ultrastructural studies. Neither adherence nor cytotoxicity was induced by preincubation of microfilariae, instead of macrophages with immune serum. The serum factor which mediated adherence and cytotoxicity was heat-labile, but was not a complement component. Immune absorption experiments showed that the relevant serum factor resided in the IgE class of antibody. The immune adherence to D. viteae by macrophages is stage-specific because adherence to infective larvae was not observed whether rate macrophages were preincubated in sera obtained from rats immune to microfilariae or in sera collected from animals after exposure to infective larvae.

Animals↗

PubMed1980

Homocytotropic antibody responses during murine schistosomiasis. A follow-up study of both total immunoglobulins and Schistosoma mansoni specific antibodies.

Mice infected with Schistosoma mansoni develop a high increase of homocytotropic antibodies, thought to be involved in protection. IgE and IgG1 rise differently during the course of infection. Total serum IgE levels rise between days 20 and 30 and the maximum is observed around day 50. IgG1 levels remain almost unchanged until day 50 after which they increase dramatically, reaching a peak at day 100. S. mansoni specific IgE antibodies measured by passive cutaneous anaphylaxis parallel to variations of total IgE. On the contrary, S. mansoni specific IgG1 antibodies, also measured by passive cutaneous anaphylaxis, do not parallel total IgG1; they reach a peak between days 30 and 40 and remain high until day 100.

Animals↗

PubMed1980

Circulating antigens, immune complexes and C3d levels in human schistosomiasis: relationship with Schistosoma mansoni egg output.

Circulating schistosome antigens (CSA), circulating immune complexes (CIC) and C3 breakdown product - C3d - were investigated in human schistosomiasis in comparison to the S. mansoni egg count. A close relationship was observed between the mean number of eggs/g of stool and the detection of CSA (evaluated by the radioimmunoprecipitation-PEG assay - Ripega), CIC (Clq-binding test) and C3d levels (quantitated by radial immunodiffusion). All the patients with more than 500 S. mansoni eggs/g of stool also presented antigen '4', specific of the genus Schistosoma, in the serum. A significant correlation was noticed between levels of CSA and CIC. This suggests the involvement of several schistosome antigens in the detected CIC. No relationship was noted between CIC and C3d levels. In contrast, there was a highly significant correlation between levels of CSA and C3d. The interaction between certain schistosome antigens and the complement system is discussed.

Adolescent↗

PubMed1979

[Production of monoclonal anti-Schistosoma mansoni antibodies. Preliminary study of their biological activities].

Monoclonal antibodies against Schistosoma mansoni have been produced by fusion of splenic lymphocytes from S. mansoni infected Rats and P3-X63-Ag8 BALB/c cells. In vitro and in vivo studies of the biological activities of these antibodies have led to the identification of IgE antibodies with a high reaginic activity and antibodies which in a complement dependent or eosinophil dependent system were shown to have a marked cytotoxicity for schistosomula in vitro. This methodology seems to open new perspectives for the study of antibody function in immunity against parasites as well as for the isolation of the corresponding target antigens.

Animals↗

PubMed1979