Several mechanisms may operate to raise TGF-β levels in parasite infection, such as (i) host homeostasis to minimize immunopathology in chronic infection; (ii) pathogen triggering of TGF-β production or activation; or (iii) parasite mimicry of the host cytokine to drive the same pathway as host TGF-β. The gene discussed is TGFB1; the disease is parasitic infectious disease.