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. 2021 Jan 13;11:850. doi: 10.1038/s41598-020-79664-6

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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 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/.

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DAMPs and the effects of MSCs treated with IFN-γ on renal fibrosis. (a) HMGB1 and IL-18 are members of DAMPs—HMGB1 was reported to promote the migration of MSCs, whereas IL-18 contributed to the secretion of IFN-γ. IFN-γ secreted from natural killer cells in injured tissues activates MSCs that exert anti-inflammatory effects. However, such activation require a long period of time, which delays the effect of MSCs administered for therapeutic purposes. (b) IFN-γ stimulation promotes the secretion of prostaglandin E2 from MSCs, and increased prostaglandin E2 induces polarization of immunosuppressive CD163-positive macrophages, suppressing the persistence of inflammation. MSCs treated with IFN-γ also directly inhibit profibrogenic TGF-β1/Smad signaling, leading to the prevention of fibrosis.