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J Infect Dis. 2010 Aug 15;202(3):427-35. doi: 10.1086/653738.

Interleukin 17 receptor signaling is deleterious during Toxoplasma gondii infection in susceptible BL6 mice.

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1
Unité Mixte de Recherche (UMR), 0483 Université, Institut National de la Recherche Agronomique (INRA), Immunologie Parasitaire et Vaccinologie, Biothérapies Anti-Infectieuses, Université François Rabelais, Unité de Formation et de Recherche des Sciences Pharmaceutiques, Tours, France. rachelguiton@gmail.com

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) gamma serum levels and enhanced production of IL-10 and IFN-gamma 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.

PMID:
20575661
DOI:
10.1086/653738
[Indexed for MEDLINE]
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