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. 2022 Apr 28;16:833186. doi: 10.3389/fncel.2022.833186

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Copyright © 2022 Rouillard, Hu, Sutter, Kim, Huang and Crocker.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Hypothesized model of HMGB1 inhibitory activity on OPCs in the MS demyelinated lesion environment. Graphical representation of a demyelinated lesion in the MS brain and how expression of HMGB1 negatively impacts the remyelinating potential of OPCs. The stepwise progression from the MS brain (right) to the demyelinated lesion environment (middle panel) where HMGB1 is expressed at higher concentrations, to the intracellular response of OPCs (right panel) depicting a transcriptional influence of HMGB1 on NFκB gene expression regulation. Results from this study implicate TLR2-mediated receptor activation of NFκB gene target pathways as putative negative regulators of HMGB1 in the MS brain lesion environment. Created with BioRender.