-
Views
-
Cite
Cite
Rachel Guiton, Virginie Vasseur, Sabine Charron, Marbel Torres Arias, Nathalie Van Langendonck, Dominique Buzoni-Gatel, Bernhard Ryffel, Isabelle Dimier-Poisson, Interleukin 17 Receptor Signaling Is Deleterious during Toxoplasma gondii Infection in Susceptible BL6 Mice, The Journal of Infectious Diseases, Volume 202, Issue 3, 1 August 2010, Pages 427–435, https://doi.org/10.1086/653738
- Share Icon Share
Abstract
Th17 cells are involved in host defense against several pathogens. Using interleukin (IL) 17RA-deficient mice, we demonstrated reduced ileitis with diminished neutrophil recruitment and inflammatory lesions in the ileum, in the regional lymph node, in the spleen, and in the liver at day 7 and prolonged survival after Toxoplasma gondii infection. In addition, IL-17A antibody neutralization reduced inflammation and enhanced survival in BL6 mice. Diminished inflammation is associated with augmented interferon (IFN) γ serum levels and enhanced production of IL-10 and IFN-γ in cultured splenocytes upon antigen restimulation. Finally, cyst load and inflammation in the brain at 40 days are greater in surviving BL6 mice than in IL-17RA-deficient mice. In conclusion, oral T. gondii infection increases IL-17 expression and contributes to the inflammatory response, and IL-17 neutralization has a partial protective effect against fatal T. gondii-associated inflammation.