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. 2018 Mar 30;13(3):e0195335. doi: 10.1371/journal.pone.0195335

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© 2018 Coleman et al

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Fig 6 — (A) Schematic illustrating secretion of HMGB1 and IL-1 after burn injury. HMGB1 translocates from the nucleus to the cytoplasm where it is packaged in vesicles. HMGB1 and IL-1β were increased in plasma MVs after burn injury. HMGB1/IL-1β complexes caused enhanced increases in IL-6 and IFNβ gene induction in human THP-1 monocytes. (B) Hypothetical models of enhanced immune activation by HMGB1/pro-IL-1β and HMGB1/cleaved-IL-1β complexes. Pro-IL-1β is considered inactive at the IL-1 receptor. When coupled with HMGB1, pro-IL-1β caused enhanced immune activation in a manner similar to HMGB1/cleaved IL-1β complexes.