Biomedical subjects

I M Suszko

Publications and source records attributed to I M Suszko.

At least 55 records · Page 3Linked to original sources

PubMed1976

Uptake and catabolism of antigen by alvelar macrophages of dogs with respiratory hypersensitivity. Processing of antigen by alveolar macrophages.

The ability of alveolar macrophages of dogs to bind and metabolize two antigens was studied. The antigens were ragweed antigen E (AgE) and keyhole limpet haemocyanin (KLH). These antigens were chosen because of the availability of dogs with respiratory hypersensitivity to them and because they are of very different molecular weights. It was shown that: (1) antigen processing was identical using macrophages from hypersensitive as compared with normal dogs; (2) in comparison with AgE, much more of the higher molecular weight antigen, KLH, was bound to macrophages and much less degraded during subsequent incubation, leaving a greater proportion of the antigen bound to the cell membrane; (3) respiratory cells which had taken up AgE at 0 degrees C instead of 37 degrees C and were then incubated at 37 degrees C were much more active in catabolizing bound antigen with consequently less membrane bound antigen remaining; (4) increases in catabolism of bound AgE were also found in cells from relatively recently lavaged animals; (5) there was no evidence that cytophilic antibody contributed to the uptake of AgE.

Animals↗

PubMed1975

In vitro production of IgE by lymphocytes from a patient with hyperimmunoglobulinaemia E, eosinophilia and increased lymphocytes carrying surface IgE.

The peripheral blood lymphocytes of a patient with massive hyperimmunoglobulinaemia E were used for in vitro studies. The serum IgE ranged from 140,000-210,000 u/ml. Peripheral blood lymphocytes had approximately 7% of cells staining for surface IgE. When these cells were cultured in vitro, IgE was produced as measured by the double antibody radioimmunoassay technique. The total IgE produced ranged from 140 to 484 units per 24 hr in different cultures. IgE production was greatest in the first 24 hr of culture and declined progressively thereafter. Some cultures still had measurable IgE at 48 hr. If the lymphocytes staining for surface IgE were the cells producing the IgE, it was estimated that between 1-7 and 2-8 molecules per cell per second were produced. No definite effect of concanavalin A, pokeweed mitogen or phytohaemagglutinin on in vitro IgE production could be demonstrated under the conditions of these experiments.

Cell Fractionation↗

PubMed1975

Potentiation of IgE-mediated cutaneous reactivity and blood leucocyte histamine release by deuterium oxide.

A previous study (Gillespie & Lichtenstein, 1972) demonstrated that there was potentiation of histamine release from human peripheral blood leucocytes following exposure to antigin or anti-IgE in deuterium oxide (D2O). The current study confirms the results with human leucocytes and indicates that the degree of histamine release due to anti-IgE or its potentiation by D2O appeared independent of the serum IgE concentration of the cell donor. Further studies demonstrated that the peripheral blood leucocytes from monkeys with a sufficient degree of IgE-mediated reactivity to Ascaris antigen-released histamine following exposure to that antigen. This leucocyte histamine release occurs in animals with immediate-type cutaneous and respiratory reactivity following challenge with this antigen. Peripheral blood leucocytes from certain monkeys release histamine following exposure to anti-human IgE. Both of these Rhesus leucocyte responses are potentiated by D2O. This potentiation of histamine release in vitro in two species by D2O was compared with the potentiation of cutaneous reactivity in IgE-mediated cutaneous reactions in two species. The addition of D2O to Ascaris antigen or anti-IgE increased the end-point cutaneous titres to these stimuli in Rhesus monkeys and the addition of D2O to Ascaris or ragweed antigen increased the end point cutaneous titre to these reactants in allergic dogs. D2O did not potentiate cutaneous reactivity to histamine in either dog or Rhesus monkey.

Animals↗

PubMed1974