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

M Bakhiet, T Olsson, J Mhlanga, P Büscher, N Lycke, PH Van der Meide, K Kristensson

Research output: Contribution to journalA1: Web of Science-article


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.
Original languageEnglish
JournalEuropean Journal of Immunology
Pages (from-to)1359-1364
Publication statusPublished - 1996


  • B780-tropical-medicine
  • Protozoology
  • Trypanosoma brucei
  • Immunology
  • Experimental
  • Interferon-gamma

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