Complement (C3) levels and the effect of C3 depletion in infections of Trypanosoma brucei in mice

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Abstract
Summary Circulating C3 levels and parasitaemias have been measured in four groups of mice chronically infected with Trypanosoma brucei: group A (normal); group B (irradiated, reconstituted); Group C (T cell‐deprived); and group D (T cell‐deprived, C3‐depleted by treatment with cobra venom factor). In groups A‐C, C3 levels first rose two to three times normal, C3 thus behaving as an acute phase reactant. Three weeks after infection C3 returned to normal levels for the remainder of the infection. It is thus unlikely that the severe generalized immunodepression seen in mice infected with this trypanosome, is in any way dependent upon a reduction of circulating C3. The curves of parasitaemia in all four groups of mice were essentially similar, even though in group D mice, C3 levels were reduced to about 10% of normal for the first 3 weeks of infection. From this finding, it is argued that complement has no essential role in the mechanisms whereby mice control successive variant populations of T. brucei in the blood. Variant‐specific IgM antibodies, acting as trypagglutinins, are probably all that are required to control blood stream infections.