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. 2021 Jan 7;12(1):53. doi: 10.1038/s41419-020-03283-2

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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. 7 — IL-38 was able to alleviate inflammatory responses in vitro by inhibiting poly(I:C)-induced over production of pro-inflammatory cytokines and chemokines through intracellular STAT1, STAT3, p38 MAPK, ERK1/2, MEK and NF-κB signaling pathways. IL-38 targeted genes were associated with host innate immune response to virus in vitro. In animal study, IL-38 could mitigate poly(I:C)-induced lung injury by suppressing inflammatory responses by upregulating Treg cells but downregulating Th1, Th17, NK, NKT and γδ T cells.