Fig. 1

Classical and Non-classical apoptotic mimicry. Apoptotic mimicry employed by intracellular parasites to establish and maintain infection. a PS^POS Leishmania spp. promastigotes from in vitro cultures or from phlebotomine sandflies are necessary to establish infection, due to their ability to inhibit NO production on infected macrophages. b Intracellular L. amazonensis amastigotes are able to expose PS at their surface. PS exposure is induced and maintained by the concomitant activity of arginase and iNOS. PS exposure on these parasites is a counteraction for macrophage microbicidal activity. c Toxoplasma gondii tachyzoites are able to expose PS and macrophage infection with these parasites led to iNOS degradation and parasite establishment. d Trypanosoma cruzi trypomastigotes are the infective forms produced by infected mosquitoes. These forms are the only ones capable of expose PS and establish infection due to a TGFβ-dependent inhibition of iNOS expression. Epimastigotes and amastigotes do not expose PS. e Red blood cells infected with Plasmodium spp. (iRBC) are able to adhere to endothelial cells, promoting parasite resistance in the peripheral blood. In addition, spleen macrophages are able to engulf iRBC, leading to parasite persistence inside these splenic cells. f Entamoeba histolytica trophozoites induce the apoptotic death of neutrophils (depicted here), hepatocytes, endothelial and epithelial cells. PS exposure on apoptotic cells lead to the engulfment of these cells by trophozoites, which has an impact in trophozoite nutrition and the ability to invade host tissues. In addition, trophozoites are able to engulf naturally PS^POS red blood cells, leading to similar effects. g Infected neutrophils are able to undergo apoptosis, either by physiological or infection induction. In both cases, apoptotic infected neutrophils are engulfed by macrophages, leading to macrophage alternative activation and parasite persistence and dissemination