Figure 2.

Role of monocytes in the clinical manifestations of malaria. Sequestration of infected red blood cells (iRBCs) in the vasculature of main organs (spleen, brain, placenta, or lungs) is associated with severe disease. Infiltration of immune cells and subsequent inflammation also contributes to pathogenesis. Dyserythropoiesis and lysis of uninfected RBCs and iRBCs cause severe malaria anemia too. Human monocytes infiltrate and accumulate in the vessels of those main organs. There, monocytes secrete anti- or pro-inflammatory cytokines, express surface markers or phagocytose IgG-opsonised iRBCs. Studies disagree over whether these mechanisms drive host protection or susceptibility. Similarly, mouse monocytes accumulate and drive inflammation in the brain and lung. In the mouse model of cerebral malaria, monocytes further recruit CD8⁺ and CD4⁺ cells by secreting the chemokine CXCL10. In the lung, monocyte CD11b/CD18 expression is important for parasite clearance while the integrin CD11d/CD18 expression increases permeability of the alveolar-capillary and causes lung edema. There is no clear consensus on to what extent findings in mice models of malaria infection translate to humans but human and mouse monocyte subsets play similar roles in host defense.