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. 2019 Jul 19;10:3236. doi: 10.1038/s41467-019-11137-5

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — Ab-retargeting sensitizes tumors for PD-1 checkpoint inhibition facilitating long-term survival. a Subcutaneous MC38-pSia tumors were established in Ad5-vaccinated mice. Seven days after tumor cell injection, animals were treated with an antagonistic antibody against PD-1 as monotherapy (αPD-1) or in combination with DE1scFv-pSia antibody retargeting (DE1scFv-pSia + αPD-1) or remained untreated (control). b Tumor development and survival (group size: αPD-1: n = 8, ms: 28 days; DE1scFv-pSia + αPD-1: n = 9, ms: 45 days, control: n = 5, ms: 22 days) was monitored. c Blood samples were drawn during treatment on day 13 after start of treatment, and splenocytes were stimulated with the peptide ASMTNMELM to detect CD8 T-cell responses against the Adpgk-R304M neoepitope. Responsiveness of CD8 T cells to peptide stimulation was measured via intracellular IFNγ-staining and flow cytometry. Left panel: αPD-1 vs. DE1scFv-pSia + αPD-1 (n = 9 per group). Right panel: individuals of the DE1scFv-pSia + αPD-1 treatment group were split in those showing tumor progression (n = 6) and tumor-free animals: (n = 3). d Subcutaneous MC38-pSia tumors were established in Ad5-naive mice. Tumor-bearing mice were treated by i.t. application of hTert-Ad as monotherapy with or without i.p. PD-1 immune checkpoint inhibition, and/or antibody-retargeting according to the treatment scheme. e The left panel shows the results of tumor growth monitoring and the right panel survival data (group size n = 5, except the groups 0.9 % NaCl: n = 4 and hTert-Ad: n = 7; median survival: 0.9% NaCl ms = 22; hTert-Ad: ms = 26; hTert-Ad + αPD-1: ms = 36; hTert-Ad + DE1scFv-pSia: ms = 36; hTert-Ad + αPD-1 + DE1scFv-pSia ms = undefined). Log-rank (Mantel–Cox) test was used for survival statistics in b and d. Two-tailed unpaired t test was used for statistics in c. *p ≤ 0.05; **p ≤ 0.01; ****p ≤ 0.0001. Error bars refer to standard deviation (SD). Source data are provided as a source data file