Immunity against Helminths: Interactions with the Host and the Intercurrent Infections

Figure 1

Immune mechanisms and regulation induced against Fasciola hepatica. Two main immune mechanisms are directed against F. hepatica in the liver parenchyma: (i) during the early phase of infection, classically activated macrophages may induce nitric oxide production which is toxic for the fluke. This mechanism needs to be confirmed and may be upregulated by Th1-type cytokines and downregulated by IL-10 produced by T regulatory cells. (ii) During the chronic phase of infection, antibody-dependent cellular cytotoxicity (ADCC) allows the release of toxic mediators such as major basic protein, eosinophil cationic protein, and reactive nitrogen intermediates. This mechanism is upregulated by Th2-type cytokines. T regulatory cells (Treg cells) produce IL-10 TGF𝛽 which inhibit the production and function of Th1 cytokines. They downregulate any excessive Th2 response in the immunopathogenesis of fasciolosis. Finally, alternative activated macrophage (AAM𝜙) produces molecules that are toxic to the fluke and participates in fibrosis and tissue repair.