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. 2021 Oct 27;12(11):1010. doi: 10.1038/s41419-021-04204-7

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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 — Under CCL₄-induced acute liver injury, KCs are activated and expression of intrahepatic CXCL1, CXCL2 or CCL1, CCL2, and CCL25 is increased, resulting in the recruitment of neutrophils and inflammatory monocytes, further aggravating the liver inflammation. ① Hepatocyte-derived EVs suppress the activation of KCs and decrease CXCL1 and CXCL2. Neutrophil recruitment is inhibited via reduction of intrahepatic CXCL1 and CXCL2. As a result, inflammation is suppressed by reducing ROS production. ② Hep-EV reduces the expression of chemokine receptors CCR2, CCR8, and CCR9 in bone marrow, resulting in suppression of bone marrow-derived monocyte recruitment into the liver.