Figure 3.

Immune response against Plasmodium vivax infection. Monocytes, neutrophils, and CD8⁺ T cells mediate parasite killing through production of mitochondrial reactive oxygen species (mROS), SOD, and cytotoxic granules, respectively. Parasite killing by monocyte is antibody dependent. Cytokines produced by innate cells and act on cells from adaptive immune response, shaping effector functions of CD4⁺ T helper cells and Treg. Parasite burden and cytokines are associated with symptoms and trigger the expression of chemokines, chemokine receptors and activation and inhibitory molecules. The production of IFN-gamma is probably affected by this environment. The IL-21 is also induced by P. vivax infection, leading to T follicular helper (Tfh) expansion and it is associated with antibody production by plasma cells. The number of malaria episodes are associated with increased frequencies of Tfh cells and classical memory B cells, probably impacting protection.