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

✍ Scribed by Moiz Bakhiet; Tomas Olsson; Jama Mhlanga; Philippe Büscher; Nils Lycke; Peter H. van der Meide; Krister Kristensson

• Book ID: 102825251
• Publisher: John Wiley and Sons
• Year: 1996
• Tongue: English
• Weight: 606 KB
• Volume: 26
• Category: Article
• ISSN: 0014-2980
• DOI: 10.1002/eji.1830260627

✦ Synopsis

Human and rodent interferon-y 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)-y. We now report that proliferation of 7: 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-a, IFN-p and tumor necrosis factor (TNF)-a. While rodent-pathogenic 7: 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.

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