Fig 1.
Different aspects of macrophage–Leishmania interaction.
Leishmania responds to the intramacrophagic environment by adaptive differentiation (left panel) and hijacks vital macrophage functions via release of parasite ectoproteins (such as the ectokinase casein kinase 1 isoform 2 [CK1.2]), which affect host defense mechanisms, causing immune subversion (middle panel), and modulate host metabolic pathways, promoting parasite growth (right panel).
Fig 2.
Targeting host–parasite interaction as a new venue for antileishmanial drug discovery.
Exosomal or secreted parasite factors released into the host cell likely modulate the macrophage epigenome, causing phenotypic changes that favor parasite survival, including suppression of immune functions, prolongation of host cell survival, and metabolic changes necessary for parasite proliferation. Interfering with parasite factors that act in trans on the host cell or restoration of the normal host cell epigenome will likely interfere with intracellular parasite survival and may thus be exploited for antileishmanial drug discovery.