Human and rodent interferon-gamma as a growth factor for Trypanosoma brucei

An example for the bidirectional exchange of activating signals between a pathogen and immunocompetent cells in the host is presented. Trypanosoma brucei, which include subspecies that cause African sleeping sickness, secrete a molecule that triggers lymphocytes to produce interferon (1FN)-γ. We now report that proliferation of T. brucei is stimulated in axenic cultures by IFN-y. The growth-enhancing effect on the pathogen is inhibited by anti-IFN-y receptor (R) antibodies and does not occur after exposure to other cytokines, i.e. IFN-α, IFN-β and tumor necrosis factor (TNF)-α. While rodent-pathogenic T. brucei strains are stimulated by rat IFN-y, human pathogenic strains are more potently stimulated by human IFN-y. Rat and human IFN-y can partially block each others effects. Mice with disrupted IFN-y genes have reduced parasitemia and prolonged survival, while the outcome is reversed in mice that lack the IFN-yR gene.