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. Author manuscript; available in PMC: 2010 Aug 1.
Published in final edited form as: Cancer Res. 2009 Jul 14;69(15):6331–6338. doi: 10.1158/0008-5472.CAN-08-4329

Figure 2. Elimination of CD11c+ cells enhances the efficacy of ACT.

Figure 2

(*- P<0.05; **- P<0.01; T cells - T cell transfer; IT - anti-CD11c immunotoxin). (A) Experimental design. CD45.2+mice were inoculated i.p. with tumor and treated on day 7 and day 14 of tumor progression with 1.5×106 CD45.1+ tumor-primed T cells (T cells). When relevant, tumor-bearing mice were irradiated on the first day of T cell transfer. Tumor-bearing mice were depleted of CD11c cells with the anti-CD11c immunotoxin (IT) the day prior to the initial T cell transfer and thrice weekly for two weeks thereafter. (B) ACT plus anti-CD11c immunotoxin, but not individual treatments, induced the regression of established intraperitoneal ID8-luciferase tumors (n=12 per group in 2 independent experiments). (C) ID8-Defb29/Vegf-a tumor-bearing mice receiving ACT plus IT survived significantly longer than untreated mice, or mice receiving individual treatments (n=24 mice/group, total in 4 independent experiments). (D) In vivo proliferation of transferred congenic (CD45.1+) T cells with (T+IT) or without (T) immunotoxin administration. The percentage of transferred cells at specific locations over time was determined (n=8 mice/group in 2 independent experiments).