Figure 6
In vivo antitumor efficacy of IL-12–secreting targeted T cells is dependent on autocrine IL-12 stimulation and IFNγ secretion. (A) 19mz/IL-12+ T cells derived from C57BL6 IL-12Rβ2−/− mice, compared with 19mz/IL-12+ T cells derived from syngeneic C57BL6(mCD19−/− hCD19+/−) mice failed to induce either B-cell aplasias or eradicate systemic EL4(hCD19) tumors in C57BL6(mCD19−/− hCD19+/−) mice (B). (C) Similarly, 19mz/IL-12+ T cells derived from C57BL6 IFNγ−/− mice, compared with 19mz/IL-12+ T cells derived from syngeneic C57BL6(mCD19−/− hCD19+/−) mice were unable to induce B-cell aplasias, or eradicate systemic EL4(hCD19) tumors in C57BL6(mCD19−/− hCD19+/−) mice (D). Results shown are representative of 2 independent experiments.

In vivo antitumor efficacy of IL-12–secreting targeted T cells is dependent on autocrine IL-12 stimulation and IFNγ secretion. (A) 19mz/IL-12+ T cells derived from C57BL6 IL-12Rβ2−/− mice, compared with 19mz/IL-12+ T cells derived from syngeneic C57BL6(mCD19−/− hCD19+/−) mice failed to induce either B-cell aplasias or eradicate systemic EL4(hCD19) tumors in C57BL6(mCD19−/− hCD19+/−) mice (B). (C) Similarly, 19mz/IL-12+ T cells derived from C57BL6 IFNγ−/− mice, compared with 19mz/IL-12+ T cells derived from syngeneic C57BL6(mCD19−/− hCD19+/−) mice were unable to induce B-cell aplasias, or eradicate systemic EL4(hCD19) tumors in C57BL6(mCD19−/− hCD19+/−) mice (D). Results shown are representative of 2 independent experiments.

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