This review describes the role of cytokines produced by CD4+ T cells and macrophages in response to the erythrocytic stages of P. chabaudi chabaudi and other malaria infections in mice. Since virtually all compartments of the immune system are activated during the response against malaria, the variety of cytokines produced during infection is considerable. There is, however, a clear differential expression of different cytokines during primary infection. Th1-related cytokines are predominantly produced during the acute phase of infection, and lead mainly to the induction of macrophage-derived cytokines. This antibody-independent pathway is probably on the one hand, sufficient for parasite control early in infection via macrophage-associated inflammatory responses, but can, on the other hand, also lead to the pathological consequences of infection. As the infection progresses, the pattern of cytokine production shifts towards a Th2-like response. B cells play a crucial role in this process. A major consequence of this switch to a production of Th2-related cytokines later in infection would be the down-regulation of IFN-gamma-induced macrophage activation and the promotion of antibody production by mature B cells. This suggest that the mechanism of parasite control in the later stages of infection is predominantly antibody-dependent.