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. Author manuscript; available in PMC: 2015 Mar 1.
Published in final edited form as: Cell Microbiol. 2014 Mar;16(3):344–354. doi: 10.1111/cmi.12259

Figure 2. EVs in parasites.

Figure 2

A. Plasmodium sp. P. falciparum-infected RBCs release EVs that contain multiple Maurer's cleft (MC) components. One MC component, PTP2, is essential for EV release and uptake by recipient cells. The EVs are phagocytosed and induce secretion of cytokines by macrophages. EVs can also be internalized by infected RBCs and trigger differentiation of the parasite in the recipient cell into gametocytes. B. Leishmania sp. During human infection, free-living promastigote forms and intracellular amastigotes secrete EVs that contain the parasite antigen GP63. GP63 induces host SHP-1 that down-regulates the immune response. EVs can also transferred to hepatocytes where GP63 cleaves DICER1, inhibiting the maturation of the lipid regulator miR-122, promoting growth of the parasite. C. Trichomonas vaginalis. The parasite secretes EVs that can fuse with host cells and induce secretion of IL-6 and IL-8, activating receptor expression on the surface of epithelial cells and therefore inducing parasite attachment. D. Trypanosoma cruzi. Free-living trypomastigote forms secrete vesicles containing T. cruzi antigens. When fibroblasts and cardiomyocytes adsorbe EVs they become targeted by a humoral immune response that is responsible for tissue damage. Trypomastigote forms also trigger the release of EVs from monocytes, and these monocytic EVs bind to the trypomastigotes and protect them from complement lysis by binding and neutralizing the C3 convertase.