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. 2017 Jul 19;11:201. doi: 10.3389/fncel.2017.00201

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Copyright © 2017 Cruz, Hari, Qin, Couture, Huang, Lagace, Stewart and Chen.

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) 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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Ablation of IRF2 binding protein 2 (IRF2BP2) skews microglia activation towards an inflammatory phenotype. (A) Immunoblot shows loss of IRF2BP2 protein in microglia from LysMCre/IRF2BP2flox (KO) mice. WT, littermate controls. IRF2BP2-deficient microglia have markedly increased expression of (M1) inflammatory markers inducible nitric oxide synthase (iNOS), Ccl2, and the cytokines Tumor Necrosis Factor-α (TNFα) and IL1β after lipopolysaccharide (LPS) challenge (B) but a reduced response of anti-inflammatory (M2) markers Arginase 1 (Arg1), Fizz1, Ym1 to interleukin-4 (IL4) stimulation (C). NT, non-treated. N = 3 mice/group. *p < 0.05.