TITLE

Tumor Necrosis Factor (TNF) Receptor—1 (TNFp55) Signal Transduction and Macrophage-Derived Soluble TNF Are Crucial for Nitric Oxide—Mediated Trypanosoma congolense Parasite Killing

AUTHOR(S)
Magez, Stefan; Radwanska, Magdalena; Drennan, Michael; Fick, Lizette; Baral, Toya Nath; Allie, Nasiema; Jacobs, Muazzam; Nedospasov, Sergei; Brombacher, Frank; Ryffel, Bernard; de Baetselier, Patrick
PUB. DATE
September 2007
SOURCE
Journal of Infectious Diseases;9/15/2007, Vol. 196 Issue 6, p954
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Control of Trypanosoma congolense infections requires an early cell-mediated immune response. To unravel the role of tumor necrosis factor (TNF) in this process, 6 different T. congolense strains were used in 6 different gene-deficient mouse models that included TNF-/-, TNF receptor—1 (TNFp55)-/-, and TNF receptor—2 (TNFp75)-/- mice, 2 cell type—specific TNF-/- mice, as well as TNF—knock-in mice that expressed only membrane-bound TNF. Our results indicate that soluble TNF produced by macrophages/neutrophils and TNFp55 signaling are essential and sufficient to control arasitemia. The downstream mechanism in the control of T. congolense infection depends on inducible nitric oxide synthase activation in the liver. Such a role for nitric oxide is corroborated ex vivo, because the inhibitor NG-monomethyl-L-arginine blocks the trypanolytic activity of the adherent liver cell population, whereas exogenous interferon-γ that stimulates nitric oxide production enhances parasite killing. In conclusion, the control of T. congolense infection depends on macrophage/neutrophil-derived soluble TNF and intact TNFp55 signaling, which induces trypanolytic nitric oxide.
ACCESSION #
26450031

 

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