Journal
JOURNAL OF IMMUNOLOGY
Volume 175, Issue 2, Pages 899-908Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.175.2.899
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- NIAID NIH HHS [AI 19613] Funding Source: Medline
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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 (j alpha 281(-/-)) are more resistant than C57BL/6 mice to the development of lethal ileitis. j alpha 281(-/-) mice failed to overexpress IFN-gamma in the intestine early after infection. This detrimental effect of NKT cells is blocked by treatment with a-galactosylceramide, which prevents death in C57BL/6, but not in j alpha 281(-/-), 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 a-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 Thl immune response remains uncontrolled.
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