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Trypanocidal action of macrophages

IFN-y60,61 and macrophages62 play a crucial role in the control of T. cruzi infection. ROS mediate intraphagosomal killing of T. cruzi before they escape in the cytoplasm,63,64 though they would have a limited role in controlling parasite multiplication65 owing to several antioxidant enzymes.66 However, ROS may also favor parasite entry and multiplication.67 NO is the principal effector molecule involved in macrophage-mediated killing of T. cruzi,68 at least in mouse.62 Production of NO is much slower in human monocytes than mouse macrophages. More parasites might therefore escape in the cytoplasm before being killed in the phagosome,64 resulting in less efficient NO-dependent control in humans.

NO production is triggered by IFN-y, upregulated by TNF-a and type 1 IFNs,65,69 and downregulated by IL-10 and TGF-(3 in “alternatively” activated macrophages (see Section, Modulation of immune responses by macrophages). Moreover, TGF-(3 induces polyamine synthesis that favors parasite replication and persistence.63,70

Other mechanisms also contribute to limit parasite multiplication, involving indoleamine 2,3-dioxygenase (IDO),71 the immunity-related GTPases IRG47 and


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