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Complement Alterations in Rodent Malaria
Antoniana U. Krettli
Antoniana U. Krettli
Department of Pathology and Preventive Medicine, New York University School of Medicine, 550 First Avenue, New York, New York 10016
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Victor Nussenzweig
Victor Nussenzweig
Department of Pathology and Preventive Medicine, New York University School of Medicine, 550 First Avenue, New York, New York 10016
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Ruth S. Nussenzweig
Ruth S. Nussenzweig
Department of Pathology and Preventive Medicine, New York University School of Medicine, 550 First Avenue, New York, New York 10016
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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.
Author Notes
A. U. Krettli was supported by a research fellowship from the Pan American Health Organization. Permanent address: Department of Zoology and Parasitology, Federal University of Minas Gerais, Belo Horizonte, M. G., Brazil.
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