Immunity to Plasmodium chabaudi adami in the B-cell-deficient mouse

Abstract

Immunity to malaria has a multicomponent basis which requires the participation of both T- and B-lymphocyte systems¹. Previous studies have suggested that the T-lymphocyte system has an essential role in ‘re-infection immunity’ to malaria, but that B cells and/or their products are necessary for the host to survive acute infection and to clear the blood of parasites during chronic malaria^2–4. Thus, B-cell-deficient mice and chickens died of fulminant malaria when infected with Plasmodium yoelii and Plasmodium gallinaceum, respectively^2,3,5, but when their acute infections were controlled with subcurative chemotherapy, B-cell-deficient hosts developed chronic low-grade infections and resisted challenge with homologous parasites^2,4. In contrast, athymic nude mice failed to control their endogenous P. yoelii infection after the termination of drug therapy unless they had been thymus grafted before initiation of acute infection³. We now report that Plasmodium chabaudi adami (556KA) infection in B-cell-deficient mice results in an activation of a T-cell-dependent immune mechanism which terminates acute malaria in a similar way to that seen in immunologically intact mice. Furthermore, these immunized B-cell-deficient mice were resistant to homologous challenge infection as well as infections initiated with Plasmodium vinckei, but not with P. yoelii and Plasmodium berghei.