Vascular targeting of anti-CD40 antibodies and IL-2 into autochthonous tumors enhances immunotherapy in mice
J. Clin. Invest. Juliana Hamzah, et al. 118:1691 doi:10.1172/JCI33201 [Go to this article.]

Figure 5
Adoptive T cell therapy in the presence of intratumoral inflammation. (A) Survival analyses of RIP1-Tag5 mice treated with IL-2–RGR, anti-CD40–RGR, and anti-CD40–RGR/IL-2–RGR in combination with adoptive transfers of preactivated CD4⁺ and CD8⁺ Tag-specific T cells (T) (P values compared with IgG/RGR treated controls; Figure 2B). (B) Survival of RIP1-Tag5 mice treated with anti-CD40–RGR/IL-2–RGR and ConA activated lymphocytes from C3H mice (ConA T). (C) Kaplan-Meier analyses of chimeric RIP1-Tag5 mice receiving bone marrow from CD40 knockout (CD40^–/–→RT5) or wild-type (C3H→RT5) mice and RIP1-Tag5 × CD40^–/– receiving bone marrow from wild-type mice (C3H→RT5×CD40^–/–), all treated with triple treatment (IL-2–RGR, anti-CD40–RGR, adoptive transfers of Tag-specific T cells) (n = 8–10 for all survival studies; P values compared with chimeric controls; Figure 4E). One of 2 experiments is shown. (D) RIP1-Tag5 mice at an age of 23 weeks were treated with 3 weekly injections of anti-CD40–RGR antibodies, IgG, or RGR-peptide. Tumors from control mice treated with IgG (upper panels) or RGR peptide alone (middle panels) do not show reactivity for ICAM, VCAM, or E-selectin. Anti-CD40–RGR treated RIP1-Tag5 mice show upregulation of ICAM, VCAM, and E-selectin on tumor vessels (lower panel). Original magnification, ×10. Scale bar: 100 μm.