African trypanosome infections in mice that lack the interferon-γ receptor gene: Nitric oxide-dependent and -independent suppression of T-cell proliferative responses and the development of anaemia

Academic Article


  • Infection of mice with African trypanosomes leads to a severe immunosuppression, mediated by suppressor macrophages. Using ex vivo macrophage culture and in vivo cell transfer, it has been shown that nitric oxide (NO) is a potent effector product of these cells and causes both lymphocyte unresponsiveness and dyserythropoiesis. We explored the role of NO in vivo during trypanosome infection using mice with a disrupted interferon- γ-receptor gene, which were unable to respond with macrophage activation and NO synthesis. These mice were less effective at controlling parasitaemia than the wild types, but showed an improved splenic T-cell responsiveness and reduced anaemia during the early stages of infection. The data indicate that, in the mouse, NO is a significant mediator of immunosuppression only in early infection. Beyond day 10 of infection, NO-independent mechanisms are of primary significance and the control of parasitaemia and T-cell responsiveness are not directly related.
  • Published In

  • Immunology  Journal
  • Digital Object Identifier (doi)

    Author List

  • Mabbott NA; Coulson PS; Smythies LE; Wilson RA; Sternberg JM
  • Start Page

  • 476
  • End Page

  • 480
  • Volume

  • 94
  • Issue

  • 4