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. 2021 Mar 1;9:15. doi: 10.1186/s40364-021-00265-0

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© The Author(s) 2021

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. 4 — Diversity of T/NK subsets revealed by scRNA-seq analysis. a UMAP plot of sc-RNAseq data (n = 10,096 cells) showed 10 distinct clusters. b Dot plot of differently key cell-type marker genes. c Histogram showed the fractions of different cell-type in T/NK populations for each AML patient and healthy donors’ BM cells, colored based on cell type. d Dot plot showed the transcript expression pattern of stimulation molecules and their receptors. e The Kaplan-Meier overall survival curves of TCGA AML patients grouped by specific Treg gene sets, dysfunctional/exhausted-gene set (LAG3, TIGIT, CTLA4, HAVCR2, TOX, PDCD1, CD274, PDCD1LG2), and several genes (CD274, PDCD1LG2, and BATF). + represents censored observations, and P value was calculated by multivariate Cox regression