Abstract
The mechanism of the immune suppression of mice infected with the rodent malaria parasite Plasmodium berghei yoelii has been investigated.
The clearance from the peripheral blood of carbon and 51Cr-labelled sheep erythrocytes was enhanced during the period of maximal parasitaemia and maximal immunosuppression, but the uptake of sheep erythrocytes by the spleens of infected mice did not differ significantly from the uptake by the spleens of healthy mice.
There was no uptake of aggregated human γ-globulin into germinal centre areas of the spleens of infected mice during the period of maximal immune suppression, but the ability to localize human γ-globulin returned at a time when the mice recovered immune competence.
It seems probable that acute malaria infections of mice induce a quantitative or qualitative defect in the cells responsible for transporting immune complexes into germinal centres. This defect may play a part in the immunosuppression induced by the malaria parasite.
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