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. 2018 Apr 26;9:853. doi: 10.3389/fimmu.2018.00853

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Copyright © 2018 Outlioua, Pourcelot and Arnoult.

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 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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The involvement of optineurin (OPTN) in TBK1 activation following RIG-I-like receptors or toll-like receptor (TLR) 3 stimulation. After infection, viral double-strand RNAs (dsRNAs) are sensed by RIG-I in the cytosol or TLR3 in the endosomes. The corresponding adaptors, MAVS and TRIF, trigger the formation of specific signalosomes leading to the ubiquitination of TBK1. At the Golgi apparatus, OPTN recruits ubiquitinated TBK1 via its ubiquitin-binding domain, leading to the trans-autophosphorylation of this kinase. Activated TBK1 then phosphorylates IRF3, leading to the production of type I interferons (IFNs). TBK1 may directly interact with the N-terminus part of OPTN and promotes its phosphorylation. The function of the phosphorylation of TBK1 remains to be determined.