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. 2015 Dec 9;8:73. doi: 10.3389/fnmol.2015.00073

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Copyright © 2015 Kopitar-Jerala.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and reproduction in other forums is permitted, provided the original author(s) or licensor 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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Innate receptor signaling and stefin B influence NF-κB activation and caspase-11 expression in macrophages. Stefin B could act an inhibitor of cysteine cathepsins in cytosol (1) and nucleus (2) in mitochondria (3) prevents the excessive ROS formation. Toll-like receptor (TLR) signaling is activated by TLR ligands. Signaling through TLR4 which is located in plasma membrane activate NF-κB via MyD88 dependent pathway. Moreover, caspase-11 expression is regulated by NF-κB signaling. In addition, LPS stimulation results in increased mitochondrial ROS formation. LPS stimulation could lead to non-canonical inflammasome activation of caspase-11 and caspase-1 that results in IL-1β and IL-18 processing and secretion.