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. 2005 Jul 15;175(2):899-908.
doi: 10.4049/jimmunol.175.2.899.

NKT cells are critical for the initiation of an inflammatory bowel response against Toxoplasma gondii

Catherine Ronet  1 , Sylvie Darche, Maria Leite de Moraes, Sachiko Miyake, Takashi Yamamura, Jacques A Louis, Lloyd H Kasper, Dominique Buzoni-Gatel
Affiliations

NKT cells are critical for the initiation of an inflammatory bowel response against Toxoplasma gondii

Catherine Ronet et al. J Immunol. .

Abstract

We demonstrated in this study the critical role of NKT cells in the lethal ileitis induced in C57BL/6 mice after infection with Toxoplasma gondii. This intestinal inflammation is caused by overproduction of IFN-gamma in the lamina propria. The implication of NKT cells was confirmed by the observation that NKT cell-deficient mice (Jalpha281(-/-)) are more resistant than C57BL/6 mice to the development of lethal ileitis. Jalpha281(-/-) mice failed to overexpress IFN-gamma in the intestine early after infection. This detrimental effect of NKT cells is blocked by treatment with alpha-galactosylceramide, which prevents death in C57BL/6, but not in Jalpha281(-/-), mice. This protective effect is characterized by a shift in cytokine production by NKT cells toward a Th2 profile and correlates with an increased number of mesenteric Foxp3 lymphocytes. Using chimeric mice in which only NKT cells are deficient in the IL-10 gene and mice treated with anti-CD25 mAb, we identified regulatory T cells as the source of the IL-10 required for manifestation of the protective effect of alpha-galactosylceramide treatment. Our results highlight the participation of NKT cells in the parasite clearance by shifting the cytokine profile toward a Th1 pattern and simultaneously to immunopathological manifestation when this Th1 immune response remains uncontrolled.

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