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Biomedical subjects

F Santoro

Publications and source records attributed to F Santoro.

At least 109 records · Page 6Linked to original sources
PubMed1982

Monoclonal antibodies identify the protective antigens of sporozoites of Plasmodium knowlesi.

Nine monoclonal antibodies against surface antigens of sporozoites of the simian malaria parasite Plasmodium knowlesi were produced by fusion of plasmacytoma cells with spleen cells of a mouse immunized with the parasites. Immunoprecipitation of extracts of [35S]methionine-labeled sporozoites with seven of the monoclonals identified the same three polypeptides with apparent molecular weights of 52,000 (Pk52), 50,000 (Pk50) and 42,000 (Pk42). These antigens also were recognized by serum of a rhesus monkey immunized with and protected against P. knowlesi sporozoites. Pulse--chase experiments indicated that the higher molecular weight proteins are precursors of Pk42. As shown by trypsin treatment of viable sporozoites, Pk42 is a surface antigen whereas Pk52 and Pk50 appear to be intracellular. Three of the monoclonal antibodies also reacted with a membrane antigen of sporozoites of another simian malaria, P. cynomolgi, and one monoclonal antibody reacted with sporozoites of human malaria, P. falciparum. When assayed for sporozoite neutralizing activity, most of the antibodies and their Fab fragments, which recognize Pk52, Pk50, and Pk42, abolished parasite infectivity.

Animals↗
PubMed1982

Complement-mediated leukocyte adherence to infective larvae of Dipetalonema viteae (Filarioidea): requirement for eosinophils or eosinophil products in effecting macrophage adherence.

The present study reports the existence of C-mediated adherence of eosinophils and/or macrophages to filarial infective larvae of Dipetalonema viteae. C3 molecules are present on the surface of the parasite, as shown by immunofluorescence studies. Samples of fNRS depleted of AP of complement by treatment with Zymosan A or of factor B by heating at 50 degrees C for 20 min fail to mediate cell adherence to the parasite. In contrast, fNRS inactivated for CP of complement by the chelating agent EGTA retains its activity in mediating cell adherence to the parasite. There is a significant consumption of factor B and AP of complement when infective larvae are incubated in fNHS. Consumption of C4 of the CP of complement is much lower in the same test. The adherence of macrophages cannot occur without the simultaneous presence of eosinophils, whereas eosinophils probably act alone and not in concert with macrophages. The eosinophil adherence is associated with degranulation. The damage is notably enhanced by replacing the spent eosinophil population with a newly obtained population. In the present test system, mast cells did not adhere to filarial larvae even when mast cell-rich populations were used, nor did they effect macrophage adherence when presented in association with the latter. When eosinophil-enriched cell populations containing less than 1% mast cells were used, cell adherence to filarial larvae still occurred, but the presence of 30% mast cells in such cell populations markedly increased both the rate and level of adherence. We suggest that a cell-mediated adherence and destruction dependent upon the activation of complement via AP, without a requirement for specific antibody, may represent a natural mechanism of parasite killing in a nonimmune host.

Animals↗
PubMed1981

Trypanosoma cruzi infection in B-cell-deficient rats.

The effect of neonatally initiated injections of anti-mu rabbit antiserum on immunity of rats against Trypanosoma cruzi infection was investigated in vivo. Anti-mu treatment resulted in a loss of immunoglobulin M (IgM) and IgG2a synthesis and, subsequently, of antibody production. These rats so treated were shown to be significantly more susceptible to the acute phase of the infection than the control rats treated with normal rabbit serum, as measured by increased parasitemia and mortality. These results indicate the essential role of antibodies, probably in association with complement or effector cells or both, in immunity to acute Chagas' disease.

Animals↗
PubMed1981

Correlation between circulating antigens detected by the radioimmunoprecipitation-polyethylene glycol assay (RIPEGA) and C1q-binding immune complexes in human schistosomiasis mansoni.

Circulating schistosome antigens (CSA) and circulating immune complexes (CIC) were investigated in serum from 420 patients infected with Schistosoma mansoni. The radioimmunoprecipitation-polyethylene glycol assay with [125I] anti-S. mansoni rabbit antibodies appeared as a sensitive and specific method to quantify CSA. In fact, more than 75% of the patients showed significant levels of CSA. C1q-binding CIC were also detected in 70% of subjects with schistosomiasis. In addition, a close correlation was observed between levels of CSA and CIC. These data suggest that part of the CIC present in human schistosomiasis are formed by schistosome specific antigens.

Antigen-Antibody Complex↗
PubMed1981

Circulating immune complexes in human fascioliasis. Relationship with Fasciola hepatica egg output.

Circulating immune complexes were investigated by the 125I-Clq binding test in serum from patients with fascioliasis. Only 36% of all the patients studied showed significant levels of CIC. Nevertheless, when we considered only the patients eliminating Fasciola hepatica eggs in the stool and/or with the acute phase of the infection, the detection of CIC was very higher (more than 70% of the cases). In addition, a close relationship was observed between F. hepatica egg output and the incidence of CIC. This data suggest strongly the occurrence of specific parasite antigens in the detected CIC. The involvement of CIC in the pathogenesis of the acute hepatic fascioliasis is discussed.

Animals↗