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. 2003 Aug 4;198(3):433–442. doi: 10.1084/jem.20030584

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Copyright © 2003, The Rockefeller University Press

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Figure 4. — IFN-γ produced by γδ T cells is critical for protective immune responses against tumors. (A) Development of MCA-induced tumors in bone marrow chimeras and in unmanipulated mice. Four groups of age- and sex-matched mice (B6 wild-type mice, n = 10; B6 TCRβ-deficient mice, n = 13; B6 TCRδ-deficient mice, n = 11; B6 IFN-γ–deficient mice, n = 19; all at age 6 wk), and two groups of age- and sex-matched bone marrow chimeras (experimental group, n = 9; control group, n = 8; 10 wk after reconstitution) were injected with MCA (75 μg/mouse in the flank). Animals were observed weekly and tumor size was measured with a calimeter. The percentage of mice that developed tumors is shown. Data represent mean ± SD of three independent experiments. *, P < 0.001; **, P < 0.01. (B) B16 melanoma model in bone marrow chimeras. Bone marrow chimeras reconstituted as in A were injected with 5 × 10⁴ B16 F0 cells/mouse and tumor growth was recorded. The percentage of mice that developed tumors 21 d after inoculation is shown. Data represent mean ± SD of three independent experiments. *, P < 0.001; **, P < 0.01. (C) B16 melanoma model in mice reconstituted with fetal liver cells. TCRδ^−/− mice were reconstituted with fetal liver cells either from B6 TCRβ^−/− mice (γδ⁺ IFN-γ⁺) or from TCRβ^−/− IFN-γ^−/− (γδ⁺ IFN-γ⁻). 8 wk after reconstitution, mice were inoculated with 5 × 10⁴ B16 F0 cells/mouse and tumor growth was recorded. The percentage of mice that developed tumors 21 d after inoculation is shown. Data represent mean ± SD of three independent experiments. *, P < 0.001; **, P < 0.01. (D) Time course of B16 tumor development in bone marrow chimeras (B) and fetal liver reconstituted mice (C).

Figure 4. — IFN-γ produced by γδ T cells is critical for protective immune responses against tumors. (A) Development of MCA-induced tumors in bone marrow chimeras and in unmanipulated mice. Four groups of age- and sex-matched mice (B6 wild-type mice, n = 10; B6 TCRβ-deficient mice, n = 13; B6 TCRδ-deficient mice, n = 11; B6 IFN-γ–deficient mice, n = 19; all at age 6 wk), and two groups of age- and sex-matched bone marrow chimeras (experimental group, n = 9; control group, n = 8; 10 wk after reconstitution) were injected with MCA (75 μg/mouse in the flank). Animals were observed weekly and tumor size was measured with a calimeter. The percentage of mice that developed tumors is shown. Data represent mean ± SD of three independent experiments. *, P < 0.001; **, P < 0.01. (B) B16 melanoma model in bone marrow chimeras. Bone marrow chimeras reconstituted as in A were injected with 5 × 10⁴ B16 F0 cells/mouse and tumor growth was recorded. The percentage of mice that developed tumors 21 d after inoculation is shown. Data represent mean ± SD of three independent experiments. *, P < 0.001; **, P < 0.01. (C) B16 melanoma model in mice reconstituted with fetal liver cells. TCRδ^−/− mice were reconstituted with fetal liver cells either from B6 TCRβ^−/− mice (γδ⁺ IFN-γ⁺) or from TCRβ^−/− IFN-γ^−/− (γδ⁺ IFN-γ⁻). 8 wk after reconstitution, mice were inoculated with 5 × 10⁴ B16 F0 cells/mouse and tumor growth was recorded. The percentage of mice that developed tumors 21 d after inoculation is shown. Data represent mean ± SD of three independent experiments. *, P < 0.001; **, P < 0.01. (D) Time course of B16 tumor development in bone marrow chimeras (B) and fetal liver reconstituted mice (C).