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R L Tarleton

Publications and source records attributed to R L Tarleton.

59 records · Page 4Linked to original sources

Changes in cell populations and immunoglobulin-producing cells in the spleens of mice infected with Trypanosoma cruzi: correlations with parasite-specific antibody response.

Infection of mice with Trypanosoma cruzi elicits the production of parasite-specific antibodies which reach high levels and remain elevated for at least 105 days of infection. The more susceptible C3H(He) mouse actually has a higher level of "natural" antibodies for T. cruzi but may show a greater lag time in the production of antibodies in response to infection than the more resistant C57BL/6 mouse. Comparison of the kinetics of antibody production against T. cruzi and the numbers of immunoglobulin-producing cells in the spleen during the course of infection suggests that a large number of the immunoglobulin-producing cells are probably producing antibodies directed against the parasite and are not the result of an exhaustive polyclonal B-cell activation. Cell numbers in the spleen change dramatically both in total numbers and in the percentage of different cell types during infection with T. cruzi. The percentage of T cells in the spleen remains relatively unchanged throughout infection in both mouse strains tested but numbers of Ig-positive cells decrease markedly during the acute phase of infection while macrophage numbers increase up to sixfold. Cell numbers and proportions of B cells, T cells, and macrophages return to near normal values by 105 days of infection in the C57BL/6 mouse.

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Effects of extracts of Trypanosoma cruzi on immune responses: induction of a nonspecific suppressor factor.

Extracts of epimastigotes of Trypanosoma cruzi were examined for the ability to augment or suppress in vivo and in vitro responses of mouse spleen cells. When administered to mice 4 days before immunization with sheep erythrocytes, the 12,000 X g pellet and the 104,000 X g pellet and supernatant fractions of extracts of T. cruzi had no effect on the subsequent plaque-forming cell responses. Testing of the two 104,000 X g fraction in vitro resulted in a slight dose-dependent modification of anti-sheep erythrocyte responses. Also, these two fractions had a moderate dose-dependent blastogenic effect on normal spleen cells. Most significantly, the 104,000 X g supernatant fraction elicited the production of a suppressor factor when incubated with spleen cells from infected mice. This suppressor factor was also apparent when spleen cells from infected mice were incubated with intact epimastigotes or trypomastigotes. Production of the suppressor factor was insensitive to indomethacin and, therefore, presumably was not a prostaglandin.

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Mitomycin C-treated Trypanosoma cruzi in vaccination of mice: induction of immunosuppression but not protection.

Attempts to immunize susceptible hosts against infection with Trypanosoma cruzi have generally not met with a high degree of success. In the present study, we used the antimetabolite mitomycin C to produce nonreplicating, attenuated culture forms of T. cruzi. Attempts to immunize highly susceptible C3H(He) mice with single or multiple inoculi of mitomycin C-treated trypanosomes 2 weeks before injection of infective blood-form trypomastigotes did not, however, lead to greater longevity in immunized mice over nonimmunized, control mice. It was determined that a single injection of 10(7) attenuated parasites induced a transient suppression of the immune response to sheep erythrocytes which was maximum on day 7, less on day 14, and undetectable by the 21st day after immunization. This immunosuppression to a heterologous antigen did not, however, appear to be the cause of the failure of the vaccination procedure to elicit protective immunity since mice immunized once with 10(7) mitomycin C-treated trypanosomes and challenged 30, 60, or 90 days later exhibited no greater longevity than control mice.

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Demonstration of IgG-Fc and C3 receptors on adult Schistosoma mansoni.

Previous studies have indicated that adult schistosomes have an affinity for both IgG and C; however, thorough investigations on the possible presence of receptors for these serum proteins on the adult schistosome tegument have not been attempted. The present study presents evidence for both IgG-Fc and C3 receptors on adult schistosomes. An indirect assay utilizing fluoresceinated Staphylococcus aureus was developed to detect antigen-antibody (Ag-Ab) and antigen-antibody-C (Ag-Ab-C) binding to adult parasites. Detection of Ag-Ab and Ag-Ab-C complex binding was dependent on the presence of a metabolic inhibitor in the incubation mixture presumably to prevent shedding of bound complexes. Ag-Ab complex binding required the presence of an intact Fc on the IgG of the complex and could be partially inhibited by preincubation of parasites in heat-aggregated IgG or an isolated Fc preparation. Binding of Ag-Ab-C complexes was dependent on active C3 in the C source but not on an intact Fc on the IgG of the complex. Ag-Ab-C binding could be blocked by prior incubation of parasites in heat-aggregated IgG-C but not by C alone. Binding of host serum proteins to IgG-Fc and C3 receptors on adult schistosomes may aid parasite survival by helping to prevent immune detection.

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