Abstract
Using trypanosomes labelled with [75Se]-methionine a series of experiments was conducted to investigate antibody production in mice with acute fulminating T. brucei infections. As measured by the hepatic uptake of radiolabelled parasites, we were unable to demonstrate any evidence of antibody-mediated uptake by the liver in such mice. It was concluded that this was not due to impaired macrophage function but was caused by the inability of antibody production to cope with the massive parasitaemias produced by rapidly-replicating infections so that effective opsonization of the parasites did not occur. In contrast, a train of trypanosome which causes a more chronic infection, although initially having a similar replication, although initially having a similar replication rate, subsequently switched t a slower one and thereby allowed antibody to reach levels which permitted effective opsonization. There was no evidence that the parasite caused any significant suppression of antibody responses in these acute infections since inoculation with trypanosomes of one stock at the same time as vaccination with irradiated organisms of a second stock did not prevent the development of antibody to the latter, as measured by the hepatic uptake of radiolabelled parasites.
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Selected References
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