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. 2020 Mar 13;11:1395. doi: 10.1038/s41467-020-15229-5

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© The Author(s) 2020

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. 7 — a Enhanced stimulatory potency of tumor-infiltrating DCs. Tumor-infiltrating DCs from VV-treated mice were loaded with neopeptide 4, 9, or 11, and cocultured with the neoantigens-primed T cells from mice immunized with the 11 neopeptide mixture to assess IFN-γ production; n = 3 mice. Data presented as the means ± SD. *P < 0.05, ***P < 0.001 by two-tailed Student’s t-test. b Enhanced maturation of tumor-infiltrating DCs. Using a similar treatment schedule as described in Fig. 5a, cell suspensions prepared from VV-treated tumors were analyzed by flow cytometry. c Enhanced tumor infiltration of CD103⁺ DCs. Using the same treatment schedule as in Fig. 5a, tumor cell suspensions from VV-treated mice were analyzed by FACS; n = 5 mice. Data presented as the means ± SD. **P < 0.01 by two-tailed Student’s t-test. d Intracellular staining of IL-12 and CXCL9 of CD103⁺ DCs from VV-treated tumors. e qRT-PCR analysis of CXCL10 mRNA levels in CD103⁺ DCs isolated from VV-treated tumors; n = 5 mice. Data presented as the means ± SD. **P < 0.01 by two-tailed Student’s t-test. f Neoantigens-primed T cells proliferated more efficiently in VV-iPDL1/GM-treated mice. The neoantigens-primed T cells were labeled with 5 μM CFSE and i.v. injected into VV-treated mice. Three days later, T cell proliferation was assessed by FACS. g Enhanced stimulatory effect of VV-iPDL1/GM-infected tumor cells. MC38 tumor cells infected with VVs at MOI = 1 were cocultured with the neoantigens-primed T cells. IFN-γ production (left) and T cell proliferation (right) were measured. Data presented as the means ± SD. *P < 0.05 by two-tailed Student’s t-test. h Serum of VV-iPDL1/GM-treated mice enhanced the cytolytic activity of neoantigens-primed T cells. MC38-Luc cells were cocultured with the neoantigen-specific T cells in the presence of the sera from treated MC38-bearing mice. Cytolytic activity was calculated using luciferase emission value. Data are presented as means ± SD. **P < 0.01 by two-tailed Student’s t-test. i PD-1⁺ CD8⁺ T cells isolated from VV-treated MC38 tumors were cocultured with MC38 cells in the presence of purified iPDL1 or IgG. IFN-γ⁺ frequencies of PD-1⁺ T cells were shown from one of two independent experiments.