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Fig. 1 | Malaria Journal

Fig. 1

From: Factors influencing phagocytosis of malaria parasites: the story so far

Fig. 1

Phagocytosis of Plasmodium falciparum by monocytes and neutrophils. Monocytes and neutrophils can phagocytize P. falciparum or other parasite-related products via non-opsonic phagocytosis and/or opsonic phagocytosis. Antibody-mediated opsonic phagocytosis, which involves cytophilic antibodies IgG1 and IgG3, is likely to exert protective effect by promoting parasite clearance [12]. There are three main sub-sets of monocytes according to their CD14 and CD16 receptor expression; classical, intermediate and non-classical. The intermediate/inflammatory and non-classical monocyte populations can be expanded during an infection and they are more efficient in the uptake of infected erythrocytes (IEs) for both opsonic and non-opsonic phagocytosis. Phagocytosis of opsonized IEs by monocytes requires the participation of Fcγ receptors and complement factors, while phagocytosis of unopsonized IEs involves the participation of CD36, TLR2 and TLR4 [43]. Opsonic phagocytosis of IEs, merozoites and parasite DNA by monocytes leads to the production of pro-inflammatory mediators, while non-opsonic phagocytosis does not [5, 11, 45, 46]. There are also different sub-sets of neutrophils; low and high-density neutrophils, but it is unknown if they have distinct ability in the phagocytosis of Plasmodium. Opsonic phagocytosis of merozoites and parasite digestive vacuoles by neutrophils can lead to reactive oxygen species (ROS) production [85]. The outcomes following phagocytosis of monosodium urate crystals and haemozoin (which requires the presence of platelets) by neutrophils during malaria are not known, but it can potentially result in NETosis; this requires further investigation

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