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. 2020 Jan 8;12(2):e11223. doi: 10.15252/emmm.201911223

Figure 1. TNF‐R1 on tumor vasculature is sufficient for the antitumor effect of TNF, but not for its shock‐inducing effect.

Figure 1

  1. C57BL/6 mice were inoculated with 6 × 105 B16Bl6 parental or dnTNF‐R1 cells on day 0 and treated daily with 7 μg mTNF p.l. from day 10. Tumor growth is shown as mean tumor size index (TSI) + SEM (n = 6). The line under the graph represents the treatment period.
  2. B16Bl6 tumor growth after daily p.l. treatment with 7 μg mTNF in C57BL/6J wild‐type (WT), TNF‐R1−/−, conditional TNF‐R1 reactivation knockout (p55cneo/cneo), or p55cneo/cneo mice with Cre expression in endothelium (Flk1Cre) or all cells (DelCre). Tumor growth is shown as mean TSI + SEM (n = 7 for WT and Flk1Cre, 8 for DelCre, 9 for TNF‐R1−/−, and 10 for p55cneo/cneo). The line under the graph represents the treatment period.
  3. PCR analysis for the detection of wild‐type, conditional knockout (cneo) or reactivated (lox) TNF‐R1 allele in whole tissues, lung endothelial cells (LECs), and lung single‐cell suspension depleted of CD31+ cells.
  4. Toxicity of a single i.v. bolus injection of the indicated dose of mTNF. Mean rectal body temperature + SEM and cumulative survival rates are shown (n = 4 for Flk1Cre 10 μg; 6 for DelCre 10 μg, Flk1Cre 10 μg, and p55cneo/cneo 15 μg; 7 for WT 10 μg; 9 for WT 8 μg; 10 for DelCre 20 μg; and 5 for all other groups). For continuity of the temperature graphs, dead mice were included with a temperature of 20°C.

Source data are available online for this figure.