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. 2022 Nov 28;21:211. doi: 10.1186/s12943-022-01679-6

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 5 — Tumors upregulate NMD as an immune-escape mechanism to suppress PTC-containing antigen presentation. (A) Scheme depicting the tumor mechanism of immune evasion by NMD upregulation to silence NMD-controlled neoantigens. (B) (A) Scheme of our NMD luciferase-SIINFEKL plasmid construct. Elements cloned in the plasmid (from left to right): EF-1α promoter (blue); PEST motive (violet); luciferase (yellow); SIINFEKL cDNA (green); DDCWFYFTYSVNGYNNEAIVHVVETPDCP MHC-II peptide [26], flanked by 2 cathepsin sites; β-Globin PTC-39 cassette (brown). (C) Top: Experiment schedule. Bottom: Rag2/IL2rg^-/- mice were injected with Panc02.gCtrl (right flank) or SMG1^KD (left flank) cells expressing luciferase-SIINFEKL reporter plasmid and radiance was measured over time. On day 6, 8 x 10⁶ activated OT-I splenocytes were transferred intravenously. On day 18, 50 μg of SIINFEKL peptide was administered intraperitoneally to induce OT-I reactivation. n = 5/group. (D) Scheme depicting Panc02.gCtrl injected in the right flank and SMG1^KD in the left one. (E) Images of Rag2/IL2rg^-/- mice from (B) on days 7, (F) Day 10 and (G) Day 18. (D) Radiance comparison between gCtrl and SMG1^KD on day 7 from (B) post-tumor inoculation. n = 5/group. (H) Radiance comparison between gCtrl and SMG1^KD on day 18 from (B) post-tumor inoculation. n = 5/group. (G) Radiance of Panc02 tumors from (B) on day 7 comparing gCtrl vs. SMG1^KD. (I) Radiance of Panc02 tumors from (B) on day 18 comparing gCtrl vs. SMG1^KD. (J) Rag2/IL2rg^-/- mice were injected with Panc02.gCtrl (right flank) or SMG1^KD (left flank) cells expressing luciferase-SIINFEKL reporter plasmid, radiance was measured over time. On day 6, 8 x 10⁶ activated Pmel splenocytes were transferred intravenously. Since SIINFEKL recognition cannot occur, no luciferase changes were observed. n = 6/group. (K) Caption of mice on day 7 (left) and 15 (right) from (J). (L) Radiance comparison between gCtrl and SMG1^KD on day 15 from (J) post-tumor inoculation. n = 6/group