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. 2020 Feb 6;10:1983. doi: 10.1038/s41598-020-58859-x

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© The Author(s) 2020

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Pathways transcriptionally dysregulated in MGUS- and MM- HDNs. Our work showed that MM-HDNs had increased expression of IL10RB, IFNGR1/2, TNFR1/2, TLR2, IL17RA/D. While IFN-gamma can activate IFNGR1/2 and IL10 can bind IL10RB in response to unresolved chronic inflammation, to activate STAT1 and STAT3 and promote their nuclear translocation, LPS triggers TLR2, through an adaptor complex which recruits TRAF6 to activate the TAK1 kinase complex can then activate the IKK complex leading to NFkB activation. The increased expression of TNFR1/B and component of their adaptor complex ½ can recruit several transcription factors to amplify the cascade and warrant a robust response. The genes target CD64 and ARG1 are under the transcriptional control of STAT1 and STAT3, as previously reported for other professional phagocytes. The lack of IL17RC excludes that the IL17R complex could be active, but the ligand of the overexpressed IL17RD is still unknown.