<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Veremeyko T</submitter><funding>Research Grants Council, University Grants Committee</funding><pagination>2515</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6221966</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>9</volume><pubmed_abstract>The process of macrophage polarization is involved in many pathologies such as anti-cancer immunity and autoimmune diseases. Polarized macrophages exhibit various levels of plasticity when M2/M(IL-4) macrophages are reprogrammed into an M1-like phenotype following treatment with IFNγ and/or LPS. At the same time, M1 macrophages are resistant to reprogramming in the presence of M2-like stimuli. The molecular mechanisms responsible for the macrophages polarization, plasticity of M2 macrophages, and lack of plasticity in M1 macrophages remain unknown. Here, we explored the role of Egr2 in the induction and maintenance of macrophage M1 and M2 polarization in the mouse &lt;i>in vitro&lt;/i> and &lt;i>in vivo&lt;/i> models of inflammation. Egr2 knockdown with siRNA treatment fail to upregulate either M1 or </pubmed_abstract><journal>Frontiers in immunology</journal><pubmed_title>Early Growth Response Gene-2 Is Essential for M1 and M2 Macrophage Activation and Plasticity by Modulation of the Transcription Factor CEBPβ.</pubmed_title><pmcid>PMC6221966</pmcid><funding_grant_id>24100314</funding_grant_id><pubmed_authors>Ponomarev ED</pubmed_authors><pubmed_authors>Yung AWY</pubmed_authors><pubmed_authors>Strekalova T</pubmed_authors><pubmed_authors>Anthony DC</pubmed_authors><pubmed_authors>Veremeyko T</pubmed_authors></additional><is_claimable>false</is_claimable><name>Early Growth Response Gene-2 Is Essential for M1 and M2 Macrophage Activation and Plasticity by Modulation of the Transcription Factor CEBPβ.</name><description>The process of macrophage polarization is involved in many pathologies such as anti-cancer immunity and autoimmune diseases. Polarized macrophages exhibit various levels of plasticity when M2/M(IL-4) macrophages are reprogrammed into an M1-like phenotype following treatment with IFNγ and/or LPS. At the same time, M1 macrophages are resistant to reprogramming in the presence of M2-like stimuli. The molecular mechanisms responsible for the macrophages polarization, plasticity of M2 macrophages, and lack of plasticity in M1 macrophages remain unknown. Here, we explored the role of Egr2 in the induction and maintenance of macrophage M1 and M2 polarization in the mouse &lt;i>in vitro&lt;/i> and &lt;i>in vivo&lt;/i> models of inflammation. Egr2 knockdown with siRNA treatment fail to upregulate either M1 or </description><dates><release>2018-01-01T00:00:00Z</release><publication>2018</publication><modification>2025-04-04T10:58:43.909Z</modification><creation>2019-03-27T00:13:02Z</creation></dates><accession>S-EPMC6221966</accession><cross_references><pubmed>30443252</pubmed><doi>10.3389/fimmu.2018.02515</doi></cross_references></HashMap>