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. 2021 Jan 28;12:650. doi: 10.1038/s41467-021-20941-x

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© The Author(s) 2021

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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Fig. 8 — a The transferred cDNT not only decreased CD4⁺ T cell proportion and survival and Th17 cell differentiation, but also selectively suppressed the proportion and cytokine production of liver-infiltrating M1, but not M2 macrophages. IL-10 secreted by M2 macrophages downregulated the immunosuppressive function of cDNT toward M2 macrophages. b The IL-10/IL-10R interaction could decrease Bcl-2 and Bcl-xL expression, and enhance cytochrome C leakage and caspase-3 activity, leading to decreased cDNT survival. The IL-10/IL-10R interaction also activates the PI3K/MAPK signaling pathway, which might induce the expression of the inhibitory receptor NKG2A. The inhibition of cDNT survival and the promotion of NKG2A expression by the IL-10/IL-10R interaction contribute to decreasing cDNT function.