Fig 1.
Immune system–parasite interactions during helminth infections. A, Blockade of innate sensing and alarmin production, such as inhibiting Toll-like receptor (TLR) responses of dendritic cells, thereby impairing inflammatory TH1/TH17 development, and abrogating epithelial cell production of IL-33, thereby pre-empting the type 2 response. ILC2, Type 2 innate lymphoid cell. B, Modulation of the adaptive immune response, promoting Treg cell differentiation either directly through production of TGF-β–like mimics (TGM) or indirectly by inducing host TGF-β and retinoic acid (RA) from DCs and macrophages. C, Modification of bystander immune responses in the infected host.