期刊
JOURNAL OF IMMUNOLOGY
卷 166, 期 9, 页码 5720-5725出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.166.9.5720
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This study documents a defect in IL-12-dependent IFN-gamma responses in a substrain (BlO.Q-H2-q/Sgj) of B10.Q mice that manifests as an acute susceptibility to infection by the intracellular protozoan pathogen, Toxoplasma gondii. Despite robust systemic production of IL-12, infected B10.Q/j animals fail to mount an early IFN-gamma response after parasite inoculation. Genetic experiments revealed that the host resistance and IFN-gamma production defects are determined by a single autosomal recessive locus distinct from the Stat4 gene. Nonetheless, a delayed IL-12-mediated IFN-gamma response emerges in later stages of acute infection but is unable to prevent host mortality. IL-18 administration restores, in an IL-12-dependent manner, the early IFN-gamma response and host resistance of B10.Q/j animals. These in vivo studies indicate that the partially impaired IL-12 responsiveness in B10.Q/j mice can result in defective host resistance and demonstrate a therapeutic function for IL-18 in reversing a genetically based immunodeficiency in IL-12-dependent IFN-gamma production.
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