Helminth Parasites Alter Protection against Plasmodium Infection

Figure 1

Representation of the course of Plasmodium chabaudi infection. Early infection with the erythrocytic stage is characterized by the production of proinflammatory cytokines, such as IL-12 and TNF-, and a pronounced IFN-γ response. In addition, NO produced by M helped control parasitemia (1). IFN-γ activates M-mediated responses, in particular phagocytosis and elimination of pRBC (2). CD4⁺ T cells, together with B cells, are crucial for developing efficient protection (3). Th1 production is downregulated later by an increased Th2-type immune response following primary infection (4). In a later stage of infection, after the peak parasitemia has been reached, CD4 T cells switch from a Th1 to a Th2 cytokine profile (5). This switch helps B cells produce antibodies (6). The antibodies inhibit the invasion of RBCs by the parasites, opsonize parasitized RBCs, or block pRBC adhesion to the vascular endothelium (7, 8). The slow late switch from noncytophilic (IgM and IgG2a) (7) to cytophilic subclasses (i.e., IgG1 and IgG3) (8) is involved in parasite elimination (9). However, IgE correlates with protection against severe malaria. Figure modified from Langhorne et al. 2004 [75] and Stevenson and Urban 2006 [67].