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. 2021 Sep 20;11:18587. doi: 10.1038/s41598-021-98131-4

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© The Author(s) 2021, corrected publication 2023

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 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/.

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TNFSF4-based immunotherapy may intersect with cancer stem cell signature repression. (A) Schematic figure illustrating the immune response. the immune system becomes suppressed when a carcinoma becomes aggressive. Later, when immune function inhibitors are blocked, active immune cells begin to infiltrate and exert cytotoxic activities against all tumor cells. Spearman correlations between TNFSF4 and immunoinhibitory factors (Y axis) across human cancers (X axis). The items in the column are listed in sequence as follows: ADORA2A, BTLA, CD160, CD244, CD274, CD96, CSF1R, CTLA4, HAVCR2, IDO1, IL10, IL10RB, KDR, KIR2DL1, KIR2DL3, LAG3, LGALS9, PDCD1, PDCD1LG2, PVRL2, TGFB1, TGFBR1, TIGIT, and VTCN1. The infiltrating lymphocyte functions and connective functional factors were analyzed, and both ALDH1A1 overexpression (B) and TNFSF4 overexpression (C) were correlated with more lymphocyte infiltration. Spearman correlations between TNFSF4 and kinds of lymphocytes (Y axis) across human cancers (X axis). The items in the column are listed in sequence as follows: ADORA2A, BTLA, CD160, CD244, CD274, CD96, CSF1R, CTLA4, HAVCR2, IDO1, IL10, IL10RB, KDR, KIR2DL1, KIR2DL3, LAG3, LGALS9, PDCD1, PDCD1LG2, PVRL2, TGFB1, TGFBR1, TIGIT, and VTCN1. However, infiltrating immune cells were suppressed by highly expressed immune inhibitors in cells with increased ALDH1A1 (D) or TNFSF4 expression (E). These results indicated that TNFSF4 blockade treatment could potentially reactivate the immune response and partially function through precisely inhibiting stem cells.