Modulation of Chemokine Production and Inflammatory Responses in Interferon-γ- and Tumor Necrosis Factor-R1-Deficient Mice during Trypanosoma cruzi Infection

Author:

Aliberti Júlio C.S.,Souto Janeusa T.,Marino Ana P.M.P.,Lannes-Vieira Joseli,Teixeira Mauro M.,Farber Joshua,Gazzinelli Ricardo T.,Silva João S.

Publisher

Elsevier BV

Subject

Pathology and Forensic Medicine

Reference25 articles.

1. The microbicidal activity of interferon-γ-treated macrophages against Trypanosoma cruzi involves an L-arginine-dependent, nitrogen oxide-mediated mechanism inhibitable by interleukin-10 and transforming growth factor-β;Gazzinelli;Eur J Immunol,1992

2. Release of nitric oxide during the experimental infection with Trypanosoma cruzi;Petray;Parasite Immunol,1994

3. Synergistic protection by specific antibodies and interferon against infection by Trypanosoma cruzi in vitro;Plata;Eur J Immunol,1984

4. In vivo administration of recombinant IFN-gamma induces macrophage activation, and prevents acute disease, immune suppression, and death in experimental Trypanosoma cruzi infection;Reed;J Immunol,1988

5. Endogenous IFN-γ is required for resistance to acute Trypanosoma cruzi infection in mice;Torrico;J Immunol,1991

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