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. 2019 May 8;10:1011. doi: 10.3389/fimmu.2019.01011

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Copyright © 2019 Tominello, Oliveira, Hussain, Elfert, Wells, Golden and Ismail.

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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Model of regulation of inflammasome activation by type I IFNs in Ehrlichia infection. During Ehrlichia infection, type I IFNs are thought to regulate inflammasome activation under a non-canonical fashion. Initially, Ehrlichia invade the target cell and induce TLR9/MyD88 signaling to upregulate NRLP3 complexes, pro-IL1β and pro-IL-18 via NF-κB. Type I IFNs from autocrine or paracrine sources would signal through IFNAR to upregulate GBPs and caspase-11. GBPs would disrupt vesicles containing Ehrlichia allowing the escape of ehrlichial PAMPs to the cytosol. Ehrlichial PAMPs would bind caspase-11 and subsequently induce inflammasome activation followed by secretion of mature IL-1β and IL-18 (as in the canonical pathway) and cleavage of gasdermin D resulting in pyroptosis. Direct arrow: positive regulation; blocking arrow: negative regulation; question mark (?) means hypothetical, and not experimentally proven.