<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Do T</submitter><funding>NIDDK NIH HHS</funding><funding>Rheumatology Research Foundation</funding><funding>Center of Excellence in Molecular Hematology</funding><funding>the Single Cell Phenotyping Core of the Cincinnati Rheumatic Diseases Resource Center</funding><funding>Children&amp;apos;s Hospital Research Foundation</funding><funding>National Institutes of Health</funding><funding>NIAMS NIH HHS</funding><funding>the Cincinnati Children&amp;apos;s Research Foundation</funding><funding>the Gene Expression Omnibus repository</funding><pagination>71-85</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9680651</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>103(1)</volume><pubmed_abstract>Systemic juvenile idiopathic arthritis (SJIA) is a severe childhood arthropathy with features of autoinflammation. Monocytes and macrophages in SJIA have a complex phenotype with both pro- and anti-inflammatory properties that combine features of several well characterized in vitro conditions used to activate macrophages. An important anti-inflammatory phenotype is expression of CD163, a scavenger receptor that sequesters toxic pro-inflammatory complexes that is highly expressed in both active SJIA and macrophage activation syndrome (MAS). CD163 is most strongly up-regulated by IL-10 (M(IL-10)), and not by other conditions that reflect features seen in SJIA monocytes such as M(LPS+IC). MicroRNA plays key roles in integrating cellular signals such as those in macrophage polarization, and as</pubmed_abstract><journal>Journal of leukocyte biology</journal><pubmed_title>MicroRNA networks associated with active systemic juvenile idiopathic arthritis regulate CD163 expression and anti-inflammatory functions in macrophages through two distinct mechanisms.</pubmed_title><pmcid>PMC9680651</pmcid><funding_grant_id>P01 AR048929</funding_grant_id><funding_grant_id>PO1-AR048929</funding_grant_id><funding_grant_id>P30-AR070549</funding_grant_id><funding_grant_id>P30 DK090971</funding_grant_id><funding_grant_id>P30 AR070549</funding_grant_id><funding_grant_id>GSE104853</funding_grant_id><pubmed_authors>Medvedovic M</pubmed_authors><pubmed_authors>Thornton S</pubmed_authors><pubmed_authors>Grom AA</pubmed_authors><pubmed_authors>Shen N</pubmed_authors><pubmed_authors>Bennett M</pubmed_authors><pubmed_authors>Schulert GS</pubmed_authors><pubmed_authors>Tan R</pubmed_authors><pubmed_authors>Do T</pubmed_authors></additional><is_claimable>false</is_claimable><name>MicroRNA networks associated with active systemic juvenile idiopathic arthritis regulate CD163 expression and anti-inflammatory functions in macrophages through two distinct mechanisms.</name><description>Systemic juvenile idiopathic arthritis (SJIA) is a severe childhood arthropathy with features of autoinflammation. Monocytes and macrophages in SJIA have a complex phenotype with both pro- and anti-inflammatory properties that combine features of several well characterized in vitro conditions used to activate macrophages. An important anti-inflammatory phenotype is expression of CD163, a scavenger receptor that sequesters toxic pro-inflammatory complexes that is highly expressed in both active SJIA and macrophage activation syndrome (MAS). CD163 is most strongly up-regulated by IL-10 (M(IL-10)), and not by other conditions that reflect features seen in SJIA monocytes such as M(LPS+IC). MicroRNA plays key roles in integrating cellular signals such as those in macrophage polarization, and as</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Jan</publication><modification>2026-05-27T11:59:34.198Z</modification><creation>2024-11-13T14:24:47.82Z</creation></dates><accession>S-EPMC9680651</accession><cross_references><pubmed>29345059</pubmed><doi>10.1002/jlb.2a0317-107r</doi><doi>10.1002/JLB.2A0317-107R</doi></cross_references></HashMap>