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Genetically Resistant Mice Lacking IL-18 Gene Develop Th1 Response and Control Cutaneous Leishmania major Infection

Gina M. Monteforte, Kiyoshi Takeda, Miriam Rodriguez-Sosa, Shizuo Akira, John R. David and Abhay R. Satoskar
J Immunol June 1, 2000, 164 (11) 5890-5893; DOI: https://doi.org/10.4049/jimmunol.164.11.5890
Gina M. Monteforte
*Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115; and
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Kiyoshi Takeda
†Department of Host Defense, Osaka University, Osaka, Japan
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Miriam Rodriguez-Sosa
*Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115; and
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Shizuo Akira
†Department of Host Defense, Osaka University, Osaka, Japan
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John R. David
*Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115; and
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Abhay R. Satoskar
*Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115; and
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  • FIGURE 1.
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    FIGURE 1.

    Course of L. major infection in IL-18+/+ and IL-18−/− mice. A and B, In two independent experiments IL-18+/+ and IL-18−/− mice were inoculated with 2 × 106 L. major stationary-phase promastigotes into the right hind footpad, and lesion growth was monitored by measuring the increase in lesion size of the infected footpad and comparing it to the thickness of the uninfected left footpad. C, In the third independent experiment we compared lesion development in IL-12−/− mice to that of IL-18−/− and IL-18+/+ mice. In all three experiments, IL-18−/− mice developed larger lesions in early course of infection than IL-18+/+ mice did; however, the differences in lesion sizes were significant in experiment 2 only (B). Data are presented as mean lesion size ± SE. ∗, Statistically significant differences between groups (p < 0.05).

  • FIGURE 2.
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    FIGURE 2.

    Parasite burdens in infected footpads from L. major-infected IL-18+/+ and IL-18−/− mice determined by limiting dilution analysis. Data are expressed as mean log titer + SE. Similar results were observed in two independent experiments.

  • FIGURE 3.
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    FIGURE 3.

    Kinetics of in vitro LmAg (20 μg/ml)-induced IFN-γ (A), IL-12 (B), and IL-4 (C) production by popliteal lymph node cells from L. major-infected IL-18+/+ and IL-18−/− mice. The data are the mean of six to seven animals at each time point for two of the three experiments. ∗, Statistically significant differences between each group (p < 0.05).

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    FIGURE 4.

    Ab responses in L. major-infected IL-18+/+ and IL-18−/− mice at 2 wk and 10 wk after infection. A, LmAg-specific IgG1; and B, Lm-Ag-specific IgG2a. Data for IgG1 and IgG2a are presented as mean reciprocal endpoint titer on log scale. Three to five mice were analyzed in each group for two of the three experiments.

  • FIGURE 5.
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    FIGURE 5.

    Administration of IFN-γ neutralizing Ab to IL-18−/− mice exacerbates cutaneous L. major infection. Data are expressed as mean lesion size + SE. ∗, Statistically significant differences between each group (p < 0.05).

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The Journal of Immunology: 164 (11)
The Journal of Immunology
Vol. 164, Issue 11
1 Jun 2000
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Genetically Resistant Mice Lacking IL-18 Gene Develop Th1 Response and Control Cutaneous Leishmania major Infection
Gina M. Monteforte, Kiyoshi Takeda, Miriam Rodriguez-Sosa, Shizuo Akira, John R. David, Abhay R. Satoskar
The Journal of Immunology June 1, 2000, 164 (11) 5890-5893; DOI: 10.4049/jimmunol.164.11.5890

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Genetically Resistant Mice Lacking IL-18 Gene Develop Th1 Response and Control Cutaneous Leishmania major Infection
Gina M. Monteforte, Kiyoshi Takeda, Miriam Rodriguez-Sosa, Shizuo Akira, John R. David, Abhay R. Satoskar
The Journal of Immunology June 1, 2000, 164 (11) 5890-5893; DOI: 10.4049/jimmunol.164.11.5890
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