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. 2021 Jul 22;21:846. doi: 10.1186/s12885-021-08529-6

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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. 3 — Multi cell-type immune-modulation changes with risk progression and is mainly targeted at monocyte-derived cells. The landscape of the immune-modulation related genes encoding cellular interface-proteins (i.e. cell-surface or secreted) inferred to be differentially transcribed across CAPRA-S risk scores, grouped by cell type. A Map of the secretory (represented as circles) and cell-surface (represented as squares) protein-coding genes that are differentially transcribed across the four cell types. The data point size is proportional to the baseline transcript abundance. The colour coding represents the effect size. Genes with a similar inflection point (i.e. at what stage of the disease a transcriptional change happens) are clustered vertically (CAPRA-S risk score < =2, > 2 and < =5 and > 5). Genes are split horizontally according to their pro- or anti-inflammatory role. Genes encoding for proteins that target monocyte-derived cells are highlighted in yellow. B Statistics of the differentially transcribed genes displayed in panel (A). Top: credible interval of the association between transcript abundance and CAPRA-S risk score. Middle: inferred effect size (full dots) and baseline transcription (empty dots). Bottom: credible interval of the CAPRA-S value for the transcriptomic change (i.e. inflection point; e.g., the gene HLA − DRB5 is upregulated in late stages of the disease)