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Table 2 Priorities for future research in understanding phagocytosis during Plasmodium infection

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

Phagocytes and clinical protection
Does high phagocytosis potential of specific immune cells or their subpopulations correlate with protection and disease progression?
What parameters can be used to define ‘effective phagocytosis’ level (level that is sufficient to confer protection against clinical disease)?
Can host genetic variations lead to different expression levels of phagocytic receptors, and will these impact phagocytic potentials of phagocytes, hence leading to different disease susceptibility?
How are the expression of opsonic and non-opsonic phagocytosis receptors regulated during malaria infection and do these expressions correlate with protection/pathology?
Molecular mechanisms of phagocytosis
Are there specific phagocyte population or subpopulations that are responsible for clearing different stages of the parasites in their asexual life cycle?
Which parasite ligands specifically interact with the phagocytes, leading to immunomodulation of phagocytosis?
What are the other phagocytic receptors involved in non-opsonic phagocytosis of Plasmodium and what are the downstream consequences of this interaction?
What are the roles of host defence peptides in phagocytosis during malaria infection?
Immune activation following phagocytosis
Are there adverse consequences that may result from increased phagocytosis, such as activation of inflammation that results in endothelial-lining damage and host pathology?
Modulation of phagocytosis
How do chronic or co-infections, such as HIV, hepatitis or helminth infections, affect the phagocytic function of phagocytes in infected hosts?
Can specific compounds or therapeutics with the potential to increase the rate phagocytosis improve treatment outcomes and/or reduce clinical manifestations of malaria?
Will immunoregulatory therapeutics aimed at dampening immune responses during severe malaria decrease phagocytic capability and thus, reduce the efficiency of parasite clearance?
What are the specific immune evasion strategies employed by Plasmodium parasites to avoid phagocytosis by phagocytes?