Nitric oxide-mediated suppression of T cell responses during Trypanosoma brucei infection: Soluble trypanosome products and interferon-γ are synergistic inducers of nitric oxide synthase

Jeremy M. Sternberg*, Neil A. Mabbott

*Corresponding author for this work

Research output: Contribution to journalArticle

59 Citations (Scopus)


African trypanosome infections result in lymphocyte unresponsiveness and anemia in the mammalian host. In murine infections, these effects are mediated by suppressor macrophages releasing nitric oxide (NO). We investigated the mechanism of activation of macrophages to produce NO during trypanosomiasis in vitro. A soluble component of trypanosome lysates induced NO synthesis in peritoneal macrophage cultures only when the macrophages were co-stimulated with interferon-gamma (IFN-γ). The macrophage-activating factor was also released in a soluble form by live bloodstream-form trypanosomes, but not procyclic trypanosomes. When splenocyte cultures were exposed to IFN-γ, and trypanosomes, an NO-dependent suppression of T cell proliferation occurred. This is similar to the suppression observed in the spleens of trypanosome-infected mice, suggesting that a combination of trypanosome-released macrophage-activating factors and IFN-γ are a trigger of immune dysfunction in trypanosomiasis.

Original languageEnglish
Pages (from-to)539-543
Number of pages5
JournalEuropean Journal of Immunology
Issue number3
Publication statusPublished - 1 Mar 1996



  • Interferon-α
  • Nitric oxide
  • Trypanosoma brucei

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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