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. 2020 Mar 4;19:51. doi: 10.1186/s12943-020-01174-w

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© The Author(s) 2020

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. 8 — MIR22HG increases the CD8 T cells in CRC. a, Scatter plots showing the correlation between CD8A expression and MIR22HG expression. b, Cell-surface expression of PD-L1 and CD8A with overexpressing MIR22HG. Left panels for human cell line and right panels for mouse. c, Relative expression of Cd8a in mice treated with aPD-L1. The right panels showing the IHC staining of CD8A and SMAD2 in tumor and normal tissues of CRC. d, Left panel showing the relative expression of Cd8a in IgG/aPD-L1 + MIR22HG treated mice. Right panel showing the IHC staining of Cd8a. e, The mechanistic scheme of lncRNA MIR22HG in CRC