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. 2018 Jun 21;12:176. doi: 10.3389/fncel.2018.00176

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Copyright © 2018 Rashid, Wolf and Langmann.

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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Regulation of microglia responses by IFN-β signaling. IFN-β initiates signaling via binding to the heterodimeric IFNα/β receptor (IFNAR). IFNAR ligation triggers activation of the associated tyrosine kinases JAK1 and TYK2 which in-turn phosphorylate STAT1 and STAT2 transcription factors. STAT1 and STAT2 can also recruit IRF-9 to form a trimolecular complex IFN-stimulated gene factor 3 (ISGF3). STAT homodimers or heterodimers activate the transcription of interferon-stimulated genes (ISGs) including suppressor of cytokine signaling 1 (SOCS1) and SOCS3 as part of a negative feedback loop. SOCS1 and SOCS3 inhibit JAK/STAT and IL-6 signaling thereby preventing excessive cytokine stimulation and dampening microglia activation.