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Medientyp:
E-Artikel
Titel:
Interferon-γ and Nitric Oxide in Combination with Antibodies Are Key Protective Host Immune Factors during Trypanosoma congolense Tc13 Infections
Beteiligte:
Magez, Stefan;
Radwanska, Magdalena;
Drennan, Michael;
Fick, Lizette;
Baral, Toya Nath;
Brombacher, Frank;
De Baetselier, Patrick
Erschienen:
University of Chicago Press, 2006
Erschienen in:
The Journal of Infectious Diseases, 193 (2006) 11, Seite 1575-1583
Beschreibung:
The control of chronic Trypanosoma congolense trypanosomiasis was analyzed using several gene-deficient mouse strains. First, interferon (IFN)-γ receptor (IFN-γ-R)-deficient mice were used to show that IFN-γmediated immune activation is crucial for parasitemia control. Second, infections in major histocompatibility complex (MHC) class II-deficient mice indicate that this molecule is needed for initiation of IFN-γ and subsequent tumor necrosis factor (TNF) production. Downstream of IFN-γ-R signaling, inducible NO synthase (iNOS)-dependent trypanosome killing occurs, as is shown by the hypersusceptible phenotype of iNOS-deficient mice. Besides proinflammatory responses, B cells and, more specifically, immunoglobulin (Ig) G antibodies are crucial for parasite killing. Hence, parasitemia control is abolished in B cell-deficient mice, whereas IgM-deficient mice control the infection as efficiently as do wild-type mice. In addition, splenectomized mice that have a normal IgM response but an impaired IgG2a/3 response fail to control T. congolense infection. Collectively, these results suggest that host protective immunity against T. congolense is critically dependent on the combined action of the proinflammatory mediators/effectors IFN-γ, TNF, and NO and antiparasite IgGs.