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. 2021 Feb 26;11:145. doi: 10.1038/s41398-021-01266-1

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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. 4 — TLR4, TLR2, and TLR7 signal activation initiates with TLR binding of MyD88, and this binding is inhibited by 3α,5α-THP. This results in the inhibition of pathway activation, including TRAF6 and activated (phosphorylated) downstream members (pERK1/2, pCREB, pATF2, and pIRF7). The activated transcription factors translocate to the nucleus and initiate the production of various inflammatory mediators (IP-10, MCP-1, and TNF-α). TLR4 also binds TRIF, which is the only adaptor protein bound by TLR3, leading to the phosphorylation (activation) of IRF3. Significantly, 3α,5α-THP does not inhibit TRIF binding and its resulting signal activation.