<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>12</volume><submitter>Mena J</submitter><funding>Instituto de Salud Carlos III</funding><pubmed_abstract>Intronic single-nucleotide polymorphisms (SNPs) in the &lt;i>ANKRD55&lt;/i> gene are associated with the risk for multiple sclerosis (MS) and rheumatoid arthritis by genome-wide association studies (GWAS). The risk alleles have been linked to higher expression levels of &lt;i>ANKRD55&lt;/i> and the neighboring &lt;i>IL6ST&lt;/i> (gp130) gene in CD4&lt;sup>+&lt;/sup> T lymphocytes of healthy controls. The biological function of ANKRD55, its role in the immune system, and cellular sources of expression other than lymphocytes remain uncharacterized. Here, we show that monocytes gain capacity to express &lt;i>ANKRD55&lt;/i> during differentiation in immature monocyte-derived dendritic cells (moDCs) in the presence of interleukin (IL)-4/granulocyte-macrophage colony-stimulating factor (GM-CSF). &lt;i>ANKRD55&lt;/i> expression lev</pubmed_abstract><journal>Frontiers in immunology</journal><pagination>816930</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8801523</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Genomic Multiple Sclerosis Risk Variants Modulate the Expression of the &lt;i>ANKRD55&lt;/i>-&lt;i>IL6ST&lt;/i> Gene Region in Immature Dendritic Cells.</pubmed_title><pmcid>PMC8801523</pmcid><pubmed_authors>Antiguedad A</pubmed_authors><pubmed_authors>Lindskog C</pubmed_authors><pubmed_authors>Alvarez de Arcaya A</pubmed_authors><pubmed_authors>Midaglia L</pubmed_authors><pubmed_authors>Comabella M</pubmed_authors><pubmed_authors>Boyero S</pubmed_authors><pubmed_authors>Aldekoa A</pubmed_authors><pubmed_authors>Sanchez Menoyo JL</pubmed_authors><pubmed_authors>Villar LM</pubmed_authors><pubmed_authors>Villarrubia N</pubmed_authors><pubmed_authors>Mena J</pubmed_authors><pubmed_authors>Alloza I</pubmed_authors><pubmed_authors>Villanueva Etxebarria A</pubmed_authors><pubmed_authors>Mendibe-Bilbao MDM</pubmed_authors><pubmed_authors>Vandenbroeck K</pubmed_authors><pubmed_authors>Montalban X</pubmed_authors><pubmed_authors>Tulloch Navarro R</pubmed_authors><pubmed_authors>Malhotra S</pubmed_authors><pubmed_authors>Diez Garcia J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Genomic Multiple Sclerosis Risk Variants Modulate the Expression of the &lt;i>ANKRD55&lt;/i>-&lt;i>IL6ST&lt;/i> Gene Region in Immature Dendritic Cells.</name><description>Intronic single-nucleotide polymorphisms (SNPs) in the &lt;i>ANKRD55&lt;/i> gene are associated with the risk for multiple sclerosis (MS) and rheumatoid arthritis by genome-wide association studies (GWAS). The risk alleles have been linked to higher expression levels of &lt;i>ANKRD55&lt;/i> and the neighboring &lt;i>IL6ST&lt;/i> (gp130) gene in CD4&lt;sup>+&lt;/sup> T lymphocytes of healthy controls. The biological function of ANKRD55, its role in the immune system, and cellular sources of expression other than lymphocytes remain uncharacterized. Here, we show that monocytes gain capacity to express &lt;i>ANKRD55&lt;/i> during differentiation in immature monocyte-derived dendritic cells (moDCs) in the presence of interleukin (IL)-4/granulocyte-macrophage colony-stimulating factor (GM-CSF). &lt;i>ANKRD55&lt;/i> expression lev</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021</publication><modification>2026-05-08T18:00:15.177Z</modification><creation>2022-02-11T15:44:27.135Z</creation></dates><accession>S-EPMC8801523</accession><cross_references><pubmed>35111166</pubmed><doi>10.3389/fimmu.2021.816930</doi></cross_references></HashMap>