Table 3.

Comparison of P. chabaudi and P. falciparum immune responses

Cell type	P. falciparum	P. chabaudi
Dendritic cells	P. falciparum: unclear; suppressive at times, but activate at low doses P. vivax: sporozoites activate DCs to kill hepatic stages Produce cytokines IL-12, IL10	Activation of CD11c+CD8+DCs (Th1), and later post-peak of infection CD11c+CD8-DCs (IL-4, IL-10) Antigen is processed within a 3–4 h time frame Produce IL-12, IL6, IL-10 and TNF
Macrophages/monocytes	Monocytes phagocytose iRBCs. Macrophages sense parasite products such as GPI anchors and parasite DNA trapped in hemozoin, and produce inflammatory cytokines TNF, IL-6 and IL-12p40	Produce IL-12 – associated with resistance. Monocytes contribute to parasite clearance
CD4+ T cells	Mix of Th1 cells producing IFN-γ with lower levels of Th2 and Th17 cells Th2 cells producing IL-4 Balance of IL-10 and TNF crucial Tregs correlated with susceptibility to infection	Th1 cells produce IFN-γ; Tregs, and IL-10+ T cells regulate pathogenesis; TNF and IFN-γ are crucial for clearance but cause pathology
B cells	Cytophilic antibody (IgG1) correlates with decreased parasitemia Antibody to parasite variants correlates to exposure, protection Disorganization of splenic architecture	Produce cytophilic antibody (IgG2a in mice) and IgG1 Large short-lived component to the antibody response and temporary disorganization in splenic architecture
Memory cells	Specific Th1 cells shown to correlate with protection Memory B cells accumulate with repeated infections	Effector memory Th1 cells develop, not exhausted Functional and long-lived B cells generated