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. Author manuscript; available in PMC: 2022 Jan 4.
Published in final edited form as: Int J Cancer. 2013 Apr 11;133(7):1643–1652. doi: 10.1002/ijc.28163

Figure 4. Doxorubicin sensitizes tumors to lysis by tumor specific T cells via augmented TRAIL signaling.

Figure 4

(A) TIL killing against untreated or DOX-treated (200 ng/ml) allogeneic J82 tumors or autologous GEWA-MEL tumors in an 18 h 51Cr release assay. (B). Summary of 51Cr-release assays of allogeneic (n=3, p=0.057) and autologous (n=4, p<0.05) TIL killing of J82 and GEWA-MEL cell lines respectively. Effector-target (E:T) ratios ranged from 0.1:1–3:1 (C) Summary of TIL-mediated killing of DOX-treated J82 tumors. The figure illustrates fold change in cytotoxicity between untreated and doxorubicin-treated tumors in presence of blocking agents (unblocked is set to 1.0, white bar). Blocking agents used were concanamycin A (CMA, n=4) or neutralizing antibodies against TRAIL (n=4), Fas-ligand (n=4), NKG2D (n=3) and DNAM-1 (n=2). (D) TIL-mediated killing of GEWA tumor cells that were either untreated or treated with 200 ng/ml doxorubicin, measured in an 18h 51Cr-release assay. TILs were incubated with blocking antibody against TRAIL (10 μg/ml) 30 min prior to co-culture with tumor cells (E:T ratio = 3:1). UNT = untreated, DOX = doxorubicin-treated.