The resulting HCQ (free base) accumulates in lysosomes (acidic cellular vesicles), gets protonated, resulting in increased concentrations within lysosomes of the malaria parasite. The increased lysosomal pH interferes with the proteolytic activity of hemoglobin thus preventing the growth of the parasite. HCQ is also known to affect with the action of parasitic heme polymerase, resulting in the build-up of the toxic -hematin and kills the parasite (Figure ). In a similar fashion, HCQ accumulates in human organelles, increase their pH, which averts the dimerization of  and  chains of the major histocompatibility complex (MHC) class II, prevents antigen presentation of the cell, and decreases the inflammatory response. HCQ is also known to reduce the release of inflammatory cytokines like tumor necrosis factor (TNF) and interleukin-. A recent study has shown that during inflammatory conditions, HCQ reduces toll-like receptors (TLR) signalling, decreasing the activation of dendritic cells and the inflammatory process (Figure ). Thus, HCQ in addition to its anti-malarial properties, modulates autoimmune responses and express anti-inflammatory action at both molecular and cellular level via lysosomal inactivity membrane destabilization, and altered signalling pathways.