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In the course of rodent malaria, the ability of mouse serum to release immune complexes from lymphocytes (complex-release, or CRA), a complement dependent function, becomes profoundly altered. These alterations occur in parallel with changes in the serum levels of the third complement component (C3). A transitory but significant increase in CRA and C3 was noticed during the first 3 days after blood-induced Plasmodium berghei infection. This was followed by a progressive decrease in CRA, which was extremely low in the 2nd week after injection. At this time, C3 levels were about 25% of those found in normal mouse serum. Incubation of blood cells of malaria-infected animals with normal serum "in vitro" resulted in a significant inhibition of the CRA of the normal serum. This inhibition was shown to operate through the alternate complement pathway. In addition, a considerable proportion of hypocomplementemic malarious sera also had an inhibitory effect on the CRA of normal sera.
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