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. 1974 Feb;16(2):279–293.

The immunological response of CBA mice to Trypanosoma musculi. I. Initial control of the infection and the effect of T-cell deprivation

P Viens, G A T Targett, E Leuchars, A J S Davies
PMCID: PMC1553923  PMID: 4619878

Abstract

Trypanosoma musculi produced a self-limiting infection in CBA mice which was characterized by a phase of increasing parasitaemia, during which dividing forms of the parasite were present in the blood, and a more stable plateau phase, when only non-dividing `adult' parasites are seen. Blood parasitaemia then rapidly regressed and subsequently blood was non-infective on sub-inoculation. Infection of normal mice in this manner apparently conferred a strong and lasting immunity. Fluorescent antibody titres rose rapidly during infection and IgM, IgGl and IgG2 antibodies were synthesized simultaneously. Total immunoglobulin and IgG2 antibody titres fell following recovery from infection but relatively high and constant antibody levels were detectable for many months.

The parasitaemia in infected, T cell-deprived mice also rose rapidly and plateaued, but at a higher level than in normal mice, and deprived mice did not recover; multiplicative forms of the parasite persisted throughout the infection (up to 300+ days). Production of IgGl antibodies was markedly inhibited in the deprived mice but IgM antibody levels were normal. The effects of anti-thymocyte antisera (ATS) administration on the course of infection in normal mice were similar to those seen in thymectomized mice but the ATS-treated mice eventually recovered. Both antibody production and the elimination of parasites from the blood was delayed by ATS treatment.

Passive transfer of antiserum just before infection prolonged the pre-patent period, and the subsequent parasitaemia was markedly reduced. If intact mice were treated on the 6th day of infection with serum collected during the plateau phase of an infection the rise in parasitaemia was checked, the number of multiplicative forms in the blood was reduced and DNA synthesis was inhibited. Antiserum from recovered mice had a similar though less marked effect on the parasitaemia. Transfer of these sera to infected, T cell-deprived mice produced similar though less dramatic effects.

These results suggest that the initial control of the infection, at the `first crisis', may be due to the joint action of a thymus-dependent ablastin, which inhibits parasite reproduction, and a thymus-independent `first' trypanocidal antibody which removes newly-formed parasites.

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Selected References

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